Updated on 2024/10/23

Information

 

写真a

 
SANUI TERUKAZU
 
Organization
Kyushu University Hospital Periodontics Lecturer
School of Dentistry Department of Dentistry(Concurrent)
Graduate School of Dental Science (Concurrent)
Graduate School of Dental Science Department of Dental Science(Concurrent)
Title
Lecturer
Contact information
メールアドレス
Tel
0926426358
Profile
・研究活動 歯周炎における病態とその後に起こる歯周組織修復・再生を分子生物学レベルで解明する研究を行っている。 ・教育活動 歯学部4年生の臨床基礎実習における講義および指導、同5年生の臨床予備実習および臨床実習における指導、同6年生の臨床実習およびリサーチエクスポージャーにおける指導を行っている。 ・診療活動 九州大学病院歯周病科で、歯周病の治療を中心に、齲蝕の保存修復治療、歯髄炎・感染根管の治療を行っている。
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Degree

  • Doctor of Philosophy for Dentistry

Research Interests・Research Keywords

  • Research theme: Complex of amelogenin and GRP78 promotes periodontal tissue regeneration.

    Keyword: periodontitis amelogenin GRP78

    Research period: 2017.4 - 2022.3

  • Research theme: Antagonists of growth factor receptors, Sproutys, could be a therapeutic target for periodontitis.

    Keyword: periodontal disease, regenerative therapy, growth factor

    Research period: 2008.4 - 2010.3

  • Research theme: Analysis of the relationship between periodntal disease and cytoskelton of T lymphocytes.

    Keyword: periodontal disease, cytoskelton, T lymphocyte

    Research period: 2005.4 - 2008.3

Awards

  • 第17回(2017年度)日本歯周病学会学術賞

    2017.12   日本歯周病学会   細胞骨格制御分子を標的とした新規歯周治療法の開発に関する基礎的研究

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    細胞骨格制御分子を標的とした新規歯周治療法の開発に関する基礎的研究

  • 財団法人武田科学振興財団医学系研究奨励<臨床>助成金受賞

    2017.11   財団法人武田科学振興財団   Takeda Science Foundation

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    炎症終焉と組織再構築を誘導する次世代歯周組織再生治療薬の発明

  • 平成26年度学術研究振興基金助成金

    2014.4   久留米大学   FGF抑制因子Sprouty/Spred によるエナメル上皮腫増殖制御機構の解明

  • 2011年度上原記念生命科学財団研究奨励金受賞

    2011.12   上原記念生命科学財団   PGRP-Sによる粘膜免疫制御機構の解明

  • ICPF 2010 Best Paper Award, Co-researcher

    2010.6   International Cleft Palate Foundation   Sprouty2 Deficient Mice Exhibit Cleft Palate.

  • 第64回学会賞優秀発表賞 共同研究者

    2010.6   日本口腔科学会   Sprouty2 KO マウスが口蓋裂を呈することから、その発症メカニズムと役割について、シグナル伝達機構を中心に解析した。

  • 財団法人武田科学振興財団医学系研究奨励<生活習慣病>助成金受賞

    2009.8   財団法人武田科学振興財団   Takeda Science Foundation

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Papers

  • Combined application of geranylgeranylacetone and amelogenin promotes angiogenesis and wound healing in human periodontal ligament cells. Reviewed International journal

    Yamato H, Sanui T, Yotsumoto K, Nakao Y, Watanabe Y, Hayashi C, Aihara R, Iwashita M, Tanaka U, Taketomi T, Fukuda T, Nishimura F.

    Journal of Cellular Biochemistry   2021.2

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: doi: 10.1002/jcb.29903.

  • Amelogenin downregulates interferon gamma-induced major histocompatibility complex class II expression through suppression of euchromatin formation in the class II transactivator promoter IV region in macrophages. Reviewed International journal

    Yotsumoto K, Sanui T, Tanaka U, Yamato H, Alshargabi R, Shinjo T, Nakao Y, Watanabe Y, Hayashi C, Taketomi T, Fukuda T, Nishimura F

    Frontiers in Immunology   11   709 - 709   2020.3

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: doi.org/10.3389/fimmu.2020.00709

  • Sprouty2 Inhibition Resolves Inflammation in Periodontal Disease and Creates a Suitable Environment for Periodontal Tissue Regeneration. Reviewed

    Sanui T, Fukuda T, Tanaka U, Toyoda K, Yotsumoto K, Nakao Y, Yamato H, Taketomi T, Nishimura F

    Journal of Cell Biology & Immunology   1   101 - 101   2017.11

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    Language:English   Publishing type:Research paper (scientific journal)  

  • Roles of serum in innate immune responses of human leukocytes to synthetic lipopeptide Reviewed

    Terukazu Sanui, Masaaki Takeshita, Takao Fukuda, Urara Tanaka, Rehab Alshargabi, Yoshitomi Aida, Fusanori Nishimura

    International Immunopharmacology   50   61 - 68   2017.9

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    Tripalmitoyl-S-glyceryl-L-Cys-Ser-(Lys)4 (Pam3CSK4) is a highly conserved molecular motif found in various classes of lipoproteins. The requirement for leukocyte to respond to synthetic Pam3CSK4 were studied. Pam3CSK4 primed neutrophils for a respiratory burst in a serum-dependent manner. Pam3CSK4 upregulated CD11b, CD14, and cytochrome b558, and downregulated Leu-8. Treatment of neutrophils with anti-CD14 antibodies and treatment of serum with anti-LPS binding protein (LBP) antibodies resulted in the inhibition of priming for respiratory burst by Pam3CSK4. It should be noted that LBP could not replicate the effects of serum in priming of neutrophils for respiratory burst by Pam3CSK4. Serum LBP bound to immobilized Pam3CSK4. Pam3CSK4 induced the interleukin-8 (IL-8) production by leukocytes in a serum-dependent manner. Further, Pam3CSK4-induced priming of neutrophils for respiratory burst was not inhibited by the LPS antagonists LA-14-PP, Rhodobacter sphaeroides LPS, or E5531, and Pam3CSK4-induced IL-8 production by leukocytes was not affected by LPS antagonist, E5531, indicating that Pam3CSK4 was recognized by a different receptor than LPS. Thus, Pam3CSK4 and LPS had similar biological activities and similar requirement to act on leukocytes, but were recognized by different receptors. Serum in the action of Pam3CSK4 on leukocytes was not replicated by LBP, suggesting that Pam3CSK4 might be disaggregated by serum to result in the activation of leukocytes.

    DOI: 10.1016/j.intimp.2017.06.006

  • Adhesion attenuates respiratory burst induced by different modes of triggering in resting or LPS-primed neutrophils Reviewed

    Terukazu Sanui, Masaaki Takeshita, Takao Fukuda, Urara Tanaka, Rehab Alshargabi, Yoshitomi Aida, Fusanori Nishimura

    Immunobiology   222 ( 8-9 )   865 - 871   2017.8

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    The effects of adherence on neutrophil superoxide anion (O2 ) generation triggered by surface, soluble ligand, or adherence were studied. Resting-neutrophils adhered to the uncoated tubes resulting in O2 generation, but not on plasma-, fibrinogen-, vitronectin-, fibronectin-, laminin-, collagen-, or poly HEMA-coated surfaces. Enhanced N-formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated O2 generation by LPS-primed-neutrophils was induced by the incubation on plasma, fibrinogen, vitronectin, fibronectin, or laminin in the absence of Mg2+. In the presence of Mg2+, this response was observed in cells on collagen or poly HEMA. LPS-primed-neutrophils adhered to uncoated, BSA- or IgG-coated tubes and did not respond to fMLP, indicating that the fMLP-response of LPS-primed-neutrophils was suppressed by adherence. Upon incubation on plasma, fibrinogen, vitronectin, fibronectin in the presence of Mg2+, LPS-primed-neutrophils showed O2 generation. Upon incubation on collagen or poly HEMA, the primed-neutrophils neither generated O2 nor adhered. We found that O2 response of LPS-primed-neutrophils was attenuated depending on the time of exposure to plasma-coated surface. This attenuation was evident on plasma or fibrinogen, but not on collagen in the presence of Mg2+, indicating that O2 generation by LPS-primed-neutrophils was attenuated dependent on adherence but not on Mg2+. Thus, adhesion attenuated the O2 generation triggered by both soluble (fMLP) and insoluble (surface) stimuli.

    DOI: 10.1016/j.imbio.2017.05.001

  • Microarray analysis of the effects of amelogenin on U937 monocytic cells. Reviewed International journal

    Terukazu Sanui, 福田 隆男, 山道 研介, Kyosuke Toyoda, Urara Tanaka, 四本 かれん, 武富 孝治, 西村 英紀

    American Journal of Molecular Biology   2017.4

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  • Anti-CD14 Antibody-treated Neutrophils Respond to LPS Possible Involvement of CD14 Upregulated by Anti-CD14 Antibody Binding Reviewed

    Terukazu Sanui, Masaaki Takeshita, Takao Fukuda, Akira Haraguchi, Yoshitomi Aida, Fusanori Nishimura

    Immunological Investigations   46 ( 2 )   190 - 200   2017.2

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    CD14 and Toll-like receptor 4/MD2 (TLR4/MD2) mediate the action of LPS on neutrophils. The anti-CD14 antibody and the TLR4/MD2-antagonist, synthetic lipid IVa (LA-14-PP), are known to inhibit the response of neutrophils to LPS. We studied the role of CD14 in LPS-induced priming of neutrophils for enhanced release of the superoxide anion. The anti-CD14 antibody at much higher concentrations than required to saturate CD14 was required to inhibit priming by LPS. The inhibitory effect of the anti-CD14 antibody was overcome by LPS. After washing, anti-CD14-treated neutrophils showed upregulated CD14 upon incubation at 37°C and responded to LPS with a delayed time-course. Thus, CD14-blocked neutrophils gained responsiveness to LPS through newly upregulated CD14. These results suggested that the unbound/free anti-CD14 antibody was essential to inhibit LPS-induced priming by blocking CD14 that were newly expressed during incubation at 37°C. LA-14-PP inhibited the response of neutrophils to LPS in an anti-CD14 antibody sensitive manner. When neutrophils were treated with LA-14-PP followed by treatment with the anti-CD14 antibody, CD14 was upregulated upon warming, but priming was blocked, suggesting that TLR4/MD2 was not newly expressed by warming in association with CD14 molecules. Thus, in addition to blocking CD14, the anti-CD14 antibody was found to induce the expression of new CD14.

    DOI: 10.1080/08820139.2016.1238925

  • Biological effects of Sprouty2 inhibition in periodontal ligament cells. Reviewed International journal

    Terukazu Sanui, 福田 隆男, Urara Tanaka, Kyosuke Toyoda, 山道 研介, 張 祥翼, 武富 孝治, 西村 英紀

    Journal of Cell Signaling   1 ( 117 )   2016.7

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    DOI: 10.4172/jcs.1000117

  • Mutation of Spry2 Induces Proliferation and Differentiation of Osteoblasts but Inhibits Proliferation of Gingival Epithelial Cells Reviewed

    Terukazu Sanui, Urara Tanaka, Takao Fukuda, Kyousuke Toyoda, Takaharu Taketomi, Ryo Atomura, Kensuke Yamamichi, Fusanori Nishimura

    Journal of Cellular Biochemistry   116 ( 4 )   628 - 639   2015.4

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    Sprouty was identified as an inhibitor of the fibroblast growth factor (FGF) receptor, and Sprouty2 (Spry2) functions as a negative regulator of receptor tyrosine kinase signaling. In this study, we investigated how inhibition of Spry2 affects osteoblasts and gingival epithelial cells in periodontal tissue regeneration in vitro. Transduction of a dominant-negative mutant of Spry2 (Y55A-Spry2) enhanced basic fibroblast growth factor (bFGF)- and epidermal growth factor (EGF)-induced ERK activation in MC3T3-E1 osteoblastic cells. In contrast, it decreased their activation in GE1 cells. Consistent with these observations, Y55A-Spry2 increased osteoblast proliferation with bFGF and EGF stimulation, whereas the proliferation of Y55A-Spry2-introduced GE1 cells was decreased via the ubiquitination and degradation of EGF receptors (EGFRs). In addition, Y55A-Spry2 caused upregulation of Runx2 expression and downregulation of Twist, a negative regulator of Runx2, with treatment of bFGF and EGF, resulting in enhanced osteoblastogenesis accompanied by alkaline phosphatase activation and osteocalcin expression in MC3T3-E1 cells. These data suggest that suppression of Spry2 expression induces proliferation and differentiation of osteoblastic cells after the addition of a bFGF and EGF cocktail but inhibits proliferation in gingival epithelial cells. These in vitro experiments may provide a molecular basis for novel therapeutic approaches in periodontal tissue regeneration. Taken together, our study proposes that combined application of an inhibitor for tyrosine 55 of Spry2, bFGF, and EGF may effectively allow alveolar bone growth and block the ingrowth of gingival epithelial cells toward bony defects, biologically mimicking a barrier effect in guided tissue regeneration, with in vivo investigation in the future. J. Cell. Biochem. 116: 628-639, 2015.

    DOI: 10.1002/jcb.25014

  • Spry2 is a novel therapeutic target for periodontal tissue regeneration through fibroblast growth factor receptor signaling and epidermal growth factor signaling Invited Reviewed International journal

    讃井 彰一, 福田 隆男, 田中 麗, 豊田 敬介, 武富 孝治, 西村 英紀

    Receptors & Clinical Investigation   e597 - e597   2015.3

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    DOI: 10.14800/rci.597

  • Analysis of Streptococcus mutans biofilm proteins recognized by salivary immunoglobulin A Reviewed

    Terukazu Sanui, R. L. Gregory

    Molecular Oral Microbiology   24 ( 5 )   361 - 368   2009.10

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    Introduction: The purpose of this study was to examine the Streptococcus mutans biofilm cellular proteins recognized by immunoglobulin A (IgA) in saliva from various caries-defined populations. Methods: Biofilm and planktonic S. mutans UA159 cells were prepared. The proteins were extracted, separated by two-dimensional gel electrophoresis, transferred to blotting membranes, and probed for IgA using individual saliva samples from three groups of subjects; those who developed 0 caries (no active caries), 5-9 caries (medium), or more than 10 caries (severe) over a 12-month interval. Results: Several proteins were recognized by salivary IgA in all groups of saliva but spot distribution and intensity varied greatly between the groups, and some proteins were recognized more strongly in biofilm cells than in planktonic culture, and vice versa. Furthermore, 15 proteins were only recognized by saliva from the 'no active caries' group, and four proteins were recognized by saliva samples from subjects in all three groups. Specifically, antigen I/II was recognized less in biofilm cells by caries-free saliva compared with planktonic cells. However, salivary IgA antibody to antigen I/II was absent in blots using saliva from the 'medium caries' and 'severe caries' groups. Conclusion: The bacterial molecules recognized by caries-free saliva are significant factors for S. mutans caries formation, and their inhibition could be a therapeutic target. In addition, saliva of caries-free subjects includes significant IgA antibody against antigen I/II of S. mutans, indicating a protective mechanism. However, microorganisms may protect themselves from host immune attack by forming biofilms and decreasing expression of antigen I/II.

    DOI: 10.1111/j.1399-302X.2009.00523.x

  • DOCK2 regulates Rac activation and cytoskeletal reorganization through interaction with ELMO1 Reviewed

    Terukazu Sanui, Ayumi Inayoshi, Mayuko Noda, Eiko Iwata, Jens V. Stein, Takehiko Sasazuki, Yoshinori Fukui

    Blood   102 ( 8 )   2948 - 2950   2003.10

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    Although the migratory property of lymphocytes is critical for protective immunity, tissue infiltration of lymphocytes sometimes causes harmful immune responses. DOCK2 plays a critical role in lymphocyte migration by regulating actin cytoskeleton through Rac activation, yet the mechanism by which DOCK2 activates Rac remains unknown. We found that DOCK2 associates with engulfment and cell motility (ELMO1) through its Src-homology 3 (SH3) domain. When DOCK2 was expressed in T-hybridoma cells lacking endogenous expression of DOCK2, Rac activation and actin polymerization were induced. However, such responses were not elicited by the DOCK2 mutant lacking the region required for ELMO1 binding. On the other hand, we found that the expression of ELMO1 induces Rac activation in the plasmacytoma cells expressing DOCK2 but not ELMO1. These results indicate that the association of DOCK2 with ELMO1 is critical for DOCK2-mediated Rac activation, thereby suggesting that their association might be a therapeutic target for immunologic disorders caused by lymphocyte infiltration.

    DOI: 10.1182/blood-2003-01-0173

  • DOCK2 is essential for antigen-induced translocation of TCR and lipid rafts, but not PKC-θ and LFA-1, in T cells Reviewed

    Terukazu Sanui, Ayumi Inayoshi, Mayuko Noda, Eiko Iwata, Masahiro Oike, Takehiko Sasazuki, Yoshinori Fukui

    Immunity   19 ( 1 )   119 - 129   2003.7

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    DOCK2 is a mammalian homolog of Caenorhabditis elegans CED-5 and Drosophila melanogaster Myoblast City which are known to regulate actin cytoskeleton. DOCK2 is critical for lymphocyte migration, yet the role of DOCK2 in TCR signaling remains unclear. We show here that DOCK2 is essential for TCR-mediated Rac activation and immunological synapse formation. In DOCK2-deficient T cells, antigen-induced translocation of TCR and lipid rafts, but not PKC-θ and LFA-1, to the APC interface was severely impaired, resulting in a significant reduction of antigen-specific T cell proliferation. In addition, we found that the efficacy of both positive and negative selection was reduced in DOCK2-deficient mice. These results suggest that DOCK2 regulates T cell responsiveness through remodeling of actin cytoskeleton via Rac activation.

    DOI: 10.1016/S1074-7613(03)00169-9

  • Preoperative endovascular arterial embolization to avoid maxillary artery injury in maxillary gingival cancer surgery

    Taketomi T., Sanui T., Fukuda T., Takeshita G., Nojiri J.

    Radiology Case Reports   19 ( 8 )   3561 - 3568   2024.8   ISSN:1930-0433

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    For maxillary gingival carcinomas, especially those in the molar region, surgical resection is often performed beyond the maxillary tuberosity. Bleeding from the posterior superior alveolar or maxillary artery into the pterygoid process is difficult to stop during partial maxillary resection. Advances in catheterization and materials have enabled the embolization of various vessels. In this report, we describe two cases of maxillary gingival cancer in which preoperative endovascular arterial embolization prevented bleeding due to unexpected vascular injury, allowing for a safe surgery with minimal blood loss. This technique effectively avoids emergency hemostasis for unexpected bleeding when resecting gingival cancers in the maxillary molar region.

    DOI: 10.1016/j.radcr.2024.05.052

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  • An 84-Year-Old Man with a History of Myeloma and Biphosphonate-Related Osteonecrosis of the Jaw Treated with Preoperative Vascular Embolization Before Partial Maxillectomy

    Taketomi, T; Fukuda, T; Nojiri, J; Sanui, T

    AMERICAN JOURNAL OF CASE REPORTS   25   e943807   2024.7   eISSN:1941-5923

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    Objective: Rare disease Background: Bisphosphonates and anti-receptor activator of nuclear factor kappa B antibodies are used to treat bone diseases associated with increased osteoclast activity, including myeloma. However, they can cause osteonecrosis of the jaw, known as medication-related osteonecrosis of the jaw. This report presents a case of a patient with a history of myeloma who required posterior maxilla resection for bisphosphonate-related osteonecrosis of the jaw, in which preoperative embolization prevented unexpected bleeding related to vascular injury and allowed for a safe procedure with minimal bleeding. Case Report: An 84-year-old man presented to our department with a 3-year history of purulent drainage and bone exposure in the right maxilla. Based on the clinical findings at the initial visit, the clinical diagnosis was bisphosphonate-related osteonecrosis of the jaw, and the patient underwent a partial right maxillary osteotomy. This surgery was associated with a risk of unexpected bleeding from a branch of the maxillary artery during the posterior maxilla resection. A catheter-based embolization of the maxillary artery was performed the day before performing a partial maxillectomy to avoid unexpected bleeding risk. Thus, no abnormal bleeding occurred during partial maxillectomy, and no postoperative complications occurred for 3 years. Conclusions: In the surgical treatment of medication-related osteonecrosis of the jaw, preoperative vascular embolization of the peripheral maxillary artery beyond the middle meningeal artery bifurcation is a valuable technique for safe maxillectomy involving the posterior maxilla.

    DOI: 10.12659/AJCR.943807

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  • Scaffold-free bone-like 3D structure established through osteogenic differentiation from human gingiva-derived stem cells. Reviewed International journal

    Toyoda M, Fukuda T, Fujimoto R, Kawakami K, Hayashi C, Nakao Y, Watanabe Y, Aoki T, Shida M, Sanui T, Taguchi M, Yamamichi K, Okabe A, Okada T, Oka K, Nakayama K, Nishimura F, Kajioka S.

    Biomed Res Int   15 ( 38 )   101656 - 101656   2024.2   ISSN:2405-5808

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Biochemistry and Biophysics Reports  

    Introduction & objectives: Stem cell therapy for regenerative medicine has been sincerely investigated, but not still popular although some clinical trials show hopeful results. This therapy is suggested to be a representative candidate such as bone defect due to the accident, iatrogenic resection oncological tumor, congenital disease, and severe periodontitis in oral region. Recently, the Bio-3D printer “Regenova®” has been introduced as an innovative three-dimensional culture system, equipped scaffold-free bio-assembling techniques without any biomaterials. Therefore, we expected a mount of bone defect could be repaired by the structure established from this Bio-3D printer using osteogenic potential stem cells. Material & methods: The gingival tissue (1x1 mm) was removed from the distal part of the lower wisdom tooth of the patients who agreed our study. Human Gingival Mesenchymal Stem Cells (hGMSCs) were isolated from this tissue and cultured, since we confirmed the characteristics such as facile isolation and accelerated proliferation, further, strong potential of osteogenic-differentiation. Spheroids were formed using hGMSC in 96-well plates designed for low cell adhesion. The size of the spheroids was measured, and fluorescent immunostaining was employed to verify the expression of stem cell and apoptosis marker, and extracellular matrix. Following four weeks of bone differentiation, μCT imaging was performed. Calcification was confirmed by alizarin red and von Kossa staining. Fluorescent immunostaining was utilized to assess the expression of markers indicative of advanced bone differentiation. Results: We have established and confirmed the spheroids (∼600 μm in diameter) constructed from human GMSCs (hGMSCs) still maintain stem cell potentials and osteogenic differentiation abilities from the results that CD73 and not CD34 were expressed as stem cell positive and negative marker, respectively. These spheroids were pilled up like cylindal shape to the “Kenzan” platform of Bio-3D printer and cultured for 7days. The cylindal structure originated from compound spheroids were tried to differentiate into bone four weeks with osteogenic induction medium. The calcification of bio-3D printed bone-like structures was confirmed by alizarin red and Von Kossa staining. In addition, μCT analysis revealed that the HU (Hounsfield Unit) of the calcified structures was almost identical to that of trabecular bone. Immunofluorescent staining detected osteocalcin expression, a late-stage bone differentiation marker. Conclusion: For the first time, we have achieved the construction of a scaffold-free, bone-like luminal structure through the assembly of spheroids comprised of this hGMSCs. This success is sure to be close to the induction of clinical application against regenerative medicine especially for bone defect disease.

    DOI: 10.1016/j.bbrep.2024.101656

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  • Luteolin Is a Potential Immunomodulating Natural Compound against Pulpal Inflammation

    Kawakami Kentaro, Fukuda Takao, Toyoda Masaaki, Nakao Yuki, Hayashi Chikako, Watanabe Yukari, Aoki Tsukasa, Shinjo Takanori, Iwashita Misaki, Yamashita Akiko, Shida Miyu, Sanui Terukazu, Uchiumi Takeshi, Nishimura Fusanori

    BioMed Research International   2024   8864513   2024.1   ISSN:23146133 eISSN:23146141

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    Aim. The present study evaluated the therapeutic effects of luteolin in alleviating pulpitis of dental pulp- (DP-) derived microvesicles (MVs) via the inhibition of protein kinase R- (PKR-) mediated inflammation. Methodology. Proteomic analysis of immortalized human dental pulp (DP-1) cell-derived MVs was performed to identify PKR-associated molecules. The effect of luteolin on PKR phosphorylation in DP-1 cells and the expression of tumor necrosis factor-α (TNF-α) in THP-1 macrophage-like cells were validated. The effect of luteolin on cell proliferation was compared with that of chemical PKR inhibitors (C16 and 2-AP) and the unique commercially available sedative guaiacol-parachlorophenol. In the dog experimental pulpitis model, the pulps were treated with (1) saline, (2) guaiacol-parachlorophenol, and (3) luteolin. Sixteen teeth from four dogs were extracted, and the pulp tissues were analyzed using hematoxylin and eosin staining. Immunohistochemical staining was performed to analyze the expression of phosphorylated PKR (pPKR), myeloperoxidase (MPO), and CD68. Experimental endodontic-periodontal complex lesions were established in mouse molar through a silk ligature and simultaneous MV injection. MVs were prepared from DP-1 cells with or without pretreatment with 2-AP or luteolin. A three-dimensional microcomputed tomography analysis was performed on day 7 (n=6). Periodontal bone resorption volumes were calculated for each group (nonligated–ligated), and the ratio of bone volume to tissue volume was measured. Results. Proteomic analysis identified an endogenous PKR activator, and a protein activator of interferon-induced PKR, also known as PACT, was included in MVs. Luteolin inhibited the expressions of pPKR in DP-1 cells and TNF-α in THP-1 cells with the lowest suppression of cell proliferation. In the dog model of experimental pulpitis, luteolin treatment suppressed the expression of pPKR-, MPO-, and CD68-positive cells in pulp tissues, whereas guaiacol-parachlorophenol treatment caused coagulative necrosis and disruption. In a mouse model of endodontic-periodontal complex lesions, luteolin treatment significantly decreased MV-induced alveolar bone resorption. Conclusion. Luteolin is an effective and safe compound that inhibits PKR activation in DP-derived MVs, enabling pulp preservation.

    CiNii Research

  • Luteolin Is a Potential Immunomodulating Natural Compound against Pulpal Inflammation. Reviewed International journal

    Kawakami K, Fukuda T, Toyoda M, Nakao Y, Hayashi C, Watanabe Y, Aoki T, Shinjo T, Iwashita M, Yamashita A, Shida M, Sanui T, Uchiumi T, Nishimura F.

    Biomed Res Int   2024   8864513 - 8864513   2024.1   ISSN:2314-6133 eISSN:2314-6141

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    Aim. The present study evaluated the therapeutic effects of luteolin in alleviating pulpitis of dental pulp- (DP-) derived microvesicles (MVs) via the inhibition of protein kinase R- (PKR-) mediated inflammation. Methodology. Proteomic analysis of immortalized human dental pulp (DP-1) cell-derived MVs was performed to identify PKR-associated molecules. The effect of luteolin on PKR phosphorylation in DP-1 cells and the expression of tumor necrosis factor-α (TNF-α) in THP-1 macrophage-like cells were validated. The effect of luteolin on cell proliferation was compared with that of chemical PKR inhibitors (C16 and 2-AP) and the unique commercially available sedative guaiacol-parachlorophenol. In the dog experimental pulpitis model, the pulps were treated with (1) saline, (2) guaiacol-parachlorophenol, and (3) luteolin. Sixteen teeth from four dogs were extracted, and the pulp tissues were analyzed using hematoxylin and eosin staining. Immunohistochemical staining was performed to analyze the expression of phosphorylated PKR (pPKR), myeloperoxidase (MPO), and CD68. Experimental endodontic-periodontal complex lesions were established in mouse molar through a silk ligature and simultaneous MV injection. MVs were prepared from DP-1 cells with or without pretreatment with 2-AP or luteolin. A three-dimensional microcomputed tomography analysis was performed on day 7 (n=6). Periodontal bone resorption volumes were calculated for each group (nonligated-ligated), and the ratio of bone volume to tissue volume was measured. Results. Proteomic analysis identified an endogenous PKR activator, and a protein activator of interferon-induced PKR, also known as PACT, was included in MVs. Luteolin inhibited the expressions of pPKR in DP-1 cells and TNF-α in THP-1 cells with the lowest suppression of cell proliferation. In the dog model of experimental pulpitis, luteolin treatment suppressed the expression of pPKR-, MPO-, and CD68-positive cells in pulp tissues, whereas guaiacol-parachlorophenol treatment caused coagulative necrosis and disruption. In a mouse model of endodontic-periodontal complex lesions, luteolin treatment significantly decreased MV-induced alveolar bone resorption. Conclusion. Luteolin is an effective and safe compound that inhibits PKR activation in DP-derived MVs, enabling pulp preservation.

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  • Luteolin, chemical feature and potential use for oral disease

    Fukuda T., Kawakami K., Toyoda M., Hayashi C., Sanui T., Uchiumi T.

    Current Oral Health Reports   11 ( 4 )   290 - 296   2024

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    Purpose of Review: Luteolin, a natural polyphenolic flavone, is a bioactive compound with high thermal stability. Owing to its prominent antioxidant activity, luteolin has been reported to exert therapeutic effects on inflammation-associated diseases. This review discusses the therapeutic potential of luteolin for treating dental diseases. Recent Findings: Luteolin has multifaceted pharmacological activities, including anti-inflammatory, neuroprotective, anticancer, and cardioprotective effects. Furthermore, the antibacterial effects of luteolin are accompanied by an anti-biofilm effect. More recently, luteolin has been identified as an inhibitor of protein kinase R (PKR), which plays an essential role in inflammasome activation. In this regard, we demonstrated the potential of luteolin as a pulp sedation compound for pulpitis that acts by suppressing PKR-mediated inflammation in dental pulp cells. Summary: Although conventional dental treatments for dental caries or periodontitis largely depend on cause-related therapy, disruption of biofilms and regulation of inflammation are prerequisites for a favorable prognosis. Together with its superior anti-inflammatory and antibacterial effects, the biocompatible features of luteolin make it a promising candidate for treating dental diseases with fewer side effects.

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  • Epithelial-to-mesenchymal transition, inflammation, subsequent collagen production, and reduced proteinase expression cooperatively contribute to cyclosporin-A-induced gingival overgrowth development

    Imagawa Mio, Shinjo Takanori, Sato Kohei, Kawakami Kentaro, Zeze Tatsuro, Nishimura Yuki, Toyoda Masaaki, Chen Shuang, Ryo Naoaki, Ahmed Al-kafee, Iwashita Misaki, Yamashita Akiko, Fukuda Takao, Sanui Terukazu, Nishimura Fusanori

    Frontiers in Physiology   14   2023.12   eISSN:1664042X

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    Drug-induced gingival overgrowth (DIGO), induced by certain immunosuppressive drugs, antihypertensive agents, and antiepileptic drugs, may contribute to the formation of deeper periodontal pockets and intractableness in periodontitis. To date, multiple factors such as enhanced matrix production, inflammation, and reduced matrix degradation might be involved in the pathogenesis of DIGO. We have previously reported that SPOCK-1, a heparan sulfate proteoglycan, could affect gingival thickening by promoting epithelial-to-mesenchymal transition (EMT) in gingival keratinocytes. However, few studies have investigated whether a combination of these factors enhances the DIGO phenotype in animal models. Therefore, we investigated whether SPOCK-1, periodontal inflammation, and cyclosporin-A (CsA) could cooperatively promote gingival overgrowth. We first confirmed that Spock-1 overexpressing (Spock1-Tg) mice showed significantly thicker gingiva and greater alveolar bone loss than WT mice in response to ligature-induced experimental periodontitis. DIGO was induced by the combination of CsA administration and experimental periodontitis was significantly enhanced in Spock1-Tg mice compared to that in WT mice. Ligature-induced alveolar bone loss in CsA-treated Spock1-Tg mice was also significantly greater than that in CsA-treated WT mice, while being accompanied by an increase in Rankl and Col1a1 levels and a reduction in matrix metalloprotease expression. Lastly, SPOCK-1 promoted RANKL-induced osteoclast differentiation in both human peripheral blood mononuclear cells and murine macrophages, while peritoneal macrophages from Spock1-Tg mice showed less TNFα and IL-1β secretion than WT mice in response to Escherichia coli lipopolysaccharide. These results suggest that EMT, periodontal inflammation, and subsequent enhanced collagen production and reduced proteinase production contribute to CsA-induced DIGO pathogenesis.

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  • A Case of a Dentigerous Cyst in the Maxillary Sinus Treated Preoperatively with Vascular Embolization to Avoid Intraoperative Abnormal Bleeding. Reviewed International journal

    Taketomi T, Fukuda T, Takeshita G, Sanui T.

    Cureus   15 ( 12 )   e50228 - e50228   2023.12   ISSN:2168-8184 eISSN:2168-8184

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  • Epithelial-to-mesenchymal transition, inflammation, subsequent collagen production, and reduced proteinase expression cooperatively contribute to cyclosporin-A-induced gingival overgrowth development. Reviewed International journal

    Imagawa M, Shinjo T, Sato K, Kawakami K, Zeze T, Nishimura Y, Toyoda M, Chen S, Ryo N, Ahmed AK, Iwashita M, Yamashita A, Fukuda T, Sanui T, Nishimura F.

    Front Physiol   13 ( 14 )   1298813 - 1298813   2023.12   ISSN:1664-042X eISSN:1664-042X

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    Drug-induced gingival overgrowth (DIGO), induced by certain immunosuppressive drugs, antihypertensive agents, and antiepileptic drugs, may contribute to the formation of deeper periodontal pockets and intractableness in periodontitis. To date, multiple factors such as enhanced matrix production, inflammation, and reduced matrix degradation might be involved in the pathogenesis of DIGO. We have previously reported that SPOCK-1, a heparan sulfate proteoglycan, could affect gingival thickening by promoting epithelial-to-mesenchymal transition (EMT) in gingival keratinocytes. However, few studies have investigated whether a combination of these factors enhances the DIGO phenotype in animal models. Therefore, we investigated whether SPOCK-1, periodontal inflammation, and cyclosporin-A (CsA) could cooperatively promote gingival overgrowth. We first confirmed that Spock-1 overexpressing (Spock1-Tg) mice showed significantly thicker gingiva and greater alveolar bone loss than WT mice in response to ligature-induced experimental periodontitis. DIGO was induced by the combination of CsA administration and experimental periodontitis was significantly enhanced in Spock1-Tg mice compared to that in WT mice. Ligature-induced alveolar bone loss in CsA-treated Spock1-Tg mice was also significantly greater than that in CsA-treated WT mice, while being accompanied by an increase in Rankl and Col1a1 levels and a reduction in matrix metalloprotease expression. Lastly, SPOCK-1 promoted RANKL-induced osteoclast differentiation in both human peripheral blood mononuclear cells and murine macrophages, while peritoneal macrophages from Spock1-Tg mice showed less TNFα and IL-1β secretion than WT mice in response to Escherichia coli lipopolysaccharide. These results suggest that EMT, periodontal inflammation, and subsequent enhanced collagen production and reduced proteinase production contribute to CsA-induced DIGO pathogenesis.

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  • Endothelial Insulin Resistance Exacerbates Experimental Periodontitis. Reviewed International journal

    Zeze T, Shinjo T, Sato K, Nishimura Y, Imagawa M, Chen S, Ahmed A-K, Iwashita M, Yamashita A, Fukuda T, Sanui T, Park K, King GL, Nishimura F.

    J Dent Res   102 ( 10 )   1152 - 1161   2023.9   ISSN:0022-0345 eISSN:1544-0591

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    Epidemiological studies suggest that the severity of periodontitis is higher in people with diabetes than in healthy individuals. Insulin resistance might play a crucial role in the pathogenesis of multiple diabetic complications and is reportedly induced in the gingiva of rodents with type 2 diabetes; however, the molecular mechanisms underlying the pathogenesis of diabetes-related periodontitis remain unclear. Therefore, we aimed to investigate whether endothelial insulin resistance in the gingiva may contribute to the pathogenesis of periodontitis as well as elucidate its underlying molecular mechanisms. We demonstrated that insulin treatment downregulated lipopolysaccharide (LPS)–induced or tumor necrosis factor α (TNFα)–induced VCAM1 expression in endothelial cells (ECs) via the PI3K/Akt activating pathway, resulting in reduced cellular adhesion between ECs and leukocytes. Hyperglycemia-induced selective insulin resistance in ECs diminished the effect of insulin on LPS- or TNFα-stimulated VCAM1 expression. Vascular endothelial cell–specific insulin receptor knockout (VEIRKO) mice exhibited selective inhibition of the PI3K/Akt pathway in the gingiva and advanced experimental periodontitis-induced alveolar bone loss via upregulation of Vcam1, Tnfα, Mcp-1, Rankl, and neutrophil migration into the gingiva compared with that in the wild-type (WT) mice despite being free from diabetes. We also observed that insulin-mediated activation of FoxO1, a downstream target of Akt, was suppressed in the gingiva of VEIRKO and high-fat diet (HFD)–fed mice, hyperglycemia-treated ECs, and primary ECs from VEIRKO. Further analysis using ECs transfected with intact and mutated FoxO1, with mutations at 3 insulin-mediated phosphorylation sites (T24A, S256D, S316A), suggested that insulin-mediated regulation of VCAM1 expression and cellular adhesion of ECs with leukocytes was attenuated by mutated FoxO1 overexpression. These results suggest that insulin resistance in ECs may contribute to the progression of periodontitis via dysregulated VCAM1 expression and cellular adhesion with leukocytes, resulting from reduced activation of the PI3K/Akt/FoxO1 axis.

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  • miR-582-5p targets Skp1 and regulates NF-κB signaling-mediated inflammation. Reviewed International journal

    Li R, Sano T, Mizokami A, Fukuda T, Shinjo T, Iwashita M, Yamashita A, Sanui T, Nakatsu Y, Sotomaru Y, Asano T, Kanematsu T, Nishimura F.

    Arch Biochem Biophys   15 ( 734 )   109501 - 109501   2023.1   ISSN:0003-9861 eISSN:1096-0384

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    A well-tuned inflammatory response is crucial for an effective immune process. Nuclear factor-kappa B (NF-κB) is a key mediator of inflammatory and innate immunity responses, and its dysregulation is closely associated with immune-related diseases. MicroRNAs (miRNAs) are important inflammation modulators. However, miRNA-regulated mechanisms that implicate NF-κB activity are not fully understood. This study aimed to identify a potential miRNA that could modulate the dysregulated NF-κB signaling during inflammation. We identified miR-582-5p that was significantly downregulated in inflamed murine adipose tissues and RAW264.7 cells. S-phase kinase-associated protein 1 (SKP1), a core component of an E3 ubiquitin ligase that regulates the NF-κB pathway, was proposed as a biological target of miR-582-5p by using TargetScan. The binding of miR-582-5p to a 3′-untranslated region site on Skp1 was confirmed using a dual-luciferase reporter assay; in addition, transfection with a miR-582-5p mimic suppressed SKP1 expression in RAW264.7 cells. Importantly, exogenous miR-582-5p attenuated the production of pro-inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6 through suppressing the degradation of the NF-κB inhibitor alpha, followed by the nuclear translocation of NF-κB. Therefore, exogenously applied miR-582-5p can attenuate the NF-κB signaling pathway via targeting Skp1; this provides a prospective therapeutic strategy for treating inflammatory and immune diseases.

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  • miR-1260b inhibits periodontal bone loss by targeting ATF6β mediated regulation of ER stress

    Hayashi Chikako, Fukuda Takao, Kawakami Kentaro, Toyoda Masaaki, Nakao Yuki, Watanabe Yukari, Shinjo Takanori, Sano Tomomi, Iwashita Misaki, Yotsumoto Karen, Shida Miyu, Taketomi Takaharu, Sanui Terukazu, Uchiumi Takeshi, Kanematsu Takashi, Nishimura Fusanori

    Frontiers in Cell and Developmental Biology   10   1061216   2022.11   ISSN:2296-634X eISSN:2296634X

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    The expression profiles of exosomal microRNAs (miRNAs) are regulated by the microenvironment, and appropriate priming with mesenchymal stem cells (MSCs) is one of the strategies to enhance the paracrine potency of MSCs. Our previous work demonstrated that exosomes from tumor necrosis factor (TNF)-α-primed human gingiva-derived MSCs (GMSCs) could be a therapeutic tool against periodontitis, and that TNFα-inducible exosomal miR-1260b is essential for the inhibition of alveolar bone loss. However, the precise molecular mechanism underlying miR-1260b-mediated inhibition of osteoclastogenesis is not yet fully understood. Here, we found that the activating transcription factor (ATF)-6β, a novel miR-1260b-targeting gene, is critical for the regulation of osteoclastogenesis under endoplasmic reticulum (ER) stress. An experimental periodontal mouse model demonstrated that induction of ER stress was accompanied by enhanced ATF6β expression, and local administration of miR-1260b and ATF6β siRNA using polyethylenimine nanoparticles (PEI-NPs) significantly suppressed the periodontal bone resorption. In periodontal ligament (PDL) cells, the ER stress inducer, tunicamycin, enhanced the expression of the receptor activator of NF-κB ligand (RANKL), while miR-1260b-mediated downregulation of ATF6β caused RANKL inhibition. Furthermore, the secretome from miR-1260b/ATF6β-axis-activated PDL cells inhibited osteoclastogenesis in human CD14^+ peripheral blood-derived monocytes. These results indicate that the miR-1260b/ATF6β axis mediates the regulation of ER stress, which may be used as a novel therapeutic strategy to treat periodontal disease.

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  • miR-1260b inhibits periodontal bone loss by targeting ATF6β mediated regulation of ER stress

    Hayashi, C; Fukuda, T; Kawakami, K; Toyoda, M; Nakao, Y; Watanabe, Y; Shinjo, T; Sano, T; Iwashita, M; Yotsumoto, K; Shida, M; Taketomi, T; Sanui, T; Uchiumi, T; Kanematsu, T; Nishimura, F

    FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY   10   2022.11   ISSN:2296-634X

  • miR-1260b inhibits periodontal bone loss by targeting ATF6β mediated regulation of ER stress. Reviewed International journal

    Hayashi C, Fukuda T, Kawakami K, Toyoda M, Nakao Y, Watanabe Y, Shinjo T, Sano T, Iwashita M, Yotsumoto K, Shida M, Taketomi T, Sanui T, Uchiumi T, Kanematsu T, Nishimura F.

    Front Cell Dev Biol   30 ( 10 )   1061216. - 1061216.   2022.11

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    DOI: doi: 10.3389/fcell.2022.1061216. eCollection 2022.

  • XAF1 overexpression exacerbates diabetes by promoting pancreatic β-cell apoptosis. Reviewed International journal

    Nishimura Y, Iwashita M, Hayashi M, Shinjo T, Watanabe Y, Zeze T, Yamashita A, Fukuda T, Sanui T, Sano T, Asano T, Nishimura F.

    Acta Diabetol   59 ( 10 )   1275 - 1286   2022.10

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    DOI: doi: 10.1007/s00592-022-01930-y.

  • XAF1 overexpression exacerbates diabetes by promoting pancreatic β-cell apoptosis

    Nishimura, Y; Iwashita, M; Hayashi, M; Shinjo, T; Watanabe, Y; Zeze, T; Yamashita, A; Fukuda, T; Sanui, T; Sano, T; Asano, T; Nishimura, F

    ACTA DIABETOLOGICA   59 ( 10 )   1275 - 1286   2022.10   ISSN:0940-5429 eISSN:1432-5233

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    Aims: Pancreatic β-cell apoptosis may be involved in the onset and progression of type 2 diabetes mellitus, although its mechanism remains unclear. We previously demonstrated that macrophage-derived interferon (IFN) β induced X-linked inhibitor of apoptosis–associated factor 1 (XAF1) expression in β-cells and accelerated β-cell apoptosis in vitro. Here, we explored the effects of XAF1 on β-cell function and progression of diabetes in vivo. Methods: Pancreatic β-cell-selective XAF1 overexpressing (Xaf1 Tg) mice were generated. Xaf1 Tg mice and their wild-type (WT) littermates were fed either a normal diet or a 40% or 60% high-fat diet (HFD). The effects of β-cell XAF1 on β-cell apoptosis and exacerbation of diabetes were investigated. Results: Palmitic acid induced IFNβ expression in macrophages, and HFD intake promoted macrophage infiltration in pancreatic islets, both of which cooperatively upregulated XAF1 expression in mouse islets. Furthermore, HFD-fed Xaf1 Tg mice demonstrated increased β-cell apoptosis, lowered insulin expression, and impaired glucose tolerance compared with WT mice fed the same diet. These effects were more pronounced in the 60%HFD group than in the 40%HFD group. Conclusions: Pancreatic β-cell XAF1 expression was enhanced via HFD-induced, macrophage-derived IFNβ, which promoted β-cell apoptosis and led to a reduction in insulin secretion and progression of diabetes. To our knowledge, this is the first report to demonstrate an association between pancreatic β-cell XAF1 overexpression and exacerbation of diabetes, thus providing insight into the mechanism of β-cell mass reduction in diabetes.

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  • Basal cell adenoma of the minor salivary glands in the buccal mucosa: A case report and literature review: Basal cell adenoma of the minor salivary glands

    Taketomi T., Nakamura K., Sanui T., Fukuda T., Tominaga Y., Takase Y., Kusukawa J.

    Oral and Maxillofacial Surgery Cases   8 ( 3 )   2022.9

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    Basal cell adenoma (BCA) is a relatively rare benign tumor of the salivary glands. However, BCA rarely occurs in the minor salivary glands. Herein, we report a rare case of BCA that originated in the left buccal mucosa of a 47-year-old female. Magnetic resonance imaging revealed a mass with a diameter of 1.5 cm and a well-defined periphery in a high-signal area on a T2-weighted image. The mass was located between the buccal and masseter muscles on the left side of the face. A biopsy was performed, and the results indicated a pathological diagnosis of BCA. Thereafter, excision of the mass was performed under local anesthesia. Histopathological examination showed that the tumor was covered with a fibrous capsule and filled with basal cell-like cells that proliferated in a solid, tubular, and trabecular pattern, with no cellular atypia or infiltrative growth. Immunohistochemistry analysis revealed that the tumor cells inside the luminal-tubular structure showed positive immunoreactivity for CK1/3, whereas those outside expressed αSMA and vimentin. However, most of the tumor cells were p63-positive. The Ki-67 labeling index of the tumor was 3%. In addition to this report, we present a review of cases of salivary gland tumors reported from 1991 to date. The review of the 20 cases (including the present case) indicated that the most common sites of occurrence were the upper lip and palate (7 [35%] cases), buccal mucosa (4 [20%] cases), and alveolar region (2 [10%] cases). The most common histopathological type was the solid type (12 cases).

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  • Extracellular vesicles derived from GMSCs stimulated with TNF-α and IFN-α promote M2 macrophage polarization via enhanced CD73 and CD5L expression

    Watanabe Yukari, Fukuda Takao, Hayashi Chikako, Nakao Yuki, Toyoda Masaaki, Kawakami Kentaro, Shinjo Takanori, Iwashita Misaki, Yamato Hiroaki, Yotsumoto Karen, Taketomi Takaharu, Uchiumi Takeshi, Sanui Terukazu, Nishimura Fusanori

    Scientific Reports   12 ( 1 )   13344   2022.8   ISSN:2045-2322 eISSN:20452322

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    Immunoregulatory properties of mesenchymal stem cell (MSC)-derived extracellular vesicles (EVs) are promising. Gingival tissue-derived MSCs (GMSCs) have unique immunoregulatory capacity and secrete large amounts of EVs. Recent findings suggest that priming MSCs with inflammatory stimuli is an effective strategy for cell-free therapy. However, the precise mechanism by which the contents of EVs are customized has not been fully elucidated. Here, we show that EVs derived from GMSCs primed with a combination of two pro-inflammatory cytokines, tumor necrosis factor-α (TNF-α) and interferon-α (IFN-α), synergistically promote anti-inflammatory M2 macrophage polarization by increasing the expression of cluster of differentiation 73 (CD73) and CD5 molecule-like (CD5L). Expression of CD73 by TNF-α/IFN-α stimulation was transcriptionally upregulated by the activation of mammalian target of rapamycin signaling and nuclear translocation of hypoxia-inducible factor 1α in GMSCs. TNF-α/IFN-α treatment also significantly increased the expression of CD5L mRNA via the transcription factor DNA-binding protein inhibitor ID3 and liver X receptor. Interestingly, exosomal CD5L is a prerequisite for the synergistic effect of EVs-mediated M2 macrophage polarization. These results indicate that combined pre-licensing with TNF-α and IFN-α in GMSCs is ideal for enhancing the anti-inflammatory function of EVs, which contributes to the establishment of a therapeutic tool.

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  • Extracellular vesicles derived from GMSCs stimulated with TNF-α and IFN-α promote M2 macrophage polarization via enhanced CD73 and CD5L expression. Reviewed International journal

    Watanabe Y, Fukuda T, Hayashi C, Nakao Y, Toyoda M, Kawakami K, Shinjo T, Iwashita M, Yamato H, Yotsumoto K, Taketomi T, Uchiumi T, Sanui T, Nishimura F.

    Sci Rep   12 ( 1 )   13344. - 13344.   2022.8

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    DOI: doi: 10.1038/s41598-022-17692-0.

  • Adipose-specific C-C motif chemokine ligand (CCL) 19 overexpression drives the mice to both insulin resistance and weight gain. Reviewed International journal

    Hayashi M, Iwashita M, Nishimura Y, Shinjo T, Sano T, Yamashita A, Fukuda T, Sanui T, Asano T, Nishimura F.

    BMJ Open Diabetes Res Care   9 ( 1 )   e001871. - e001871.   2021.5

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    DOI: doi: 10.1136/bmjdrc-2020-001871.

  • Exosomes from TNF-α-treated human gingiva-drived MSCs enhance M2 macrophage polarization and inhibit periodontal bone loss. Reviewed International journal

    Nakao Y, Fukuda T, Zhang Q, Sanui T, Shinjo T, Kou X, Chen C, Liu D, Watanabe Y, Hayashi C, Yamato H, Yotsumoto K, Tanaka U, Taketomi T, Uchiumi T, Le AD, Shi S, Nishimura F.

    Acta Biomaterials   122   306 - 324   2021.3

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    DOI: doi: 10.1016/j.actbio.2020.12.046.

  • SPOCK1 induces adipose tissue maturation: New insights into the function of SPOCK1 in metabolism. Reviewed International journal

    Alshargabi R, Shinjo T, Iwashita M, Yamashita A, Sano T, Nishimura Y, Hayashi M, Zeze T, Fukuda T, Sanui T, Nishimura F.

    Biochemical and Biophysical Research Communications   533 ( 4 )   1076 - 1082   2020.12

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    DOI: doi: 10.1016/j.bbrc.2020.09.129.

  • SPOCK1 is a novel inducer of epithelial to mesenchymal transition in drug-induced gingival overgrowth. Reviewed International journal

    Alshargabi R, Sano T, Yamashita A, Takano A, Sanada T, Iwashita M, Shinjo T, Fukuda T, Sanui T, Kishida S, Nishimura F.

    Scientific Reports   10 ( 1 )   9785 - 9785   2020.6

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    DOI: doi: 10.1038/s41598-020-66660-z.

  • Ccr7 null mice are protected against diet-induced obesity via Ucp1 upregulation and enhanced energy expenditure. Reviewed International journal

    Sano T, Sanada T, Sotomaru Y, Shinjo T, Iwashita M, Yamashita A, Fukuda T, Sanui T, Asano T, Kanematsu T, Nishimura F

    Nutrition & Metabolism   4 ( 16 )   43 - 43   2019.7

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  • Sprouty2 is involved in the control of osteoblast proliferation and differentiation through the FGF and BMP signaling pathways. Reviewed International journal

    Taketomi T, Onimura T, Yoshiga D, Muratsu D, Sanui T, Fukuda T, Kusukawa J, Nakamura S

    Cell Biology International   42 ( 9 )   1106 - 1114   2018.9

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    DOI: 10.1002/cbin.10876.

  • Amelogenin induces M2 macrophage polarisation via PGE2/cAMP signalling pathway Reviewed

    Kensuke Yamamichi, Takao Fukuda, Terukazu Sanui, Kyousuke Toyoda, Urara Tanaka, Yuki Nakao, Karen Yotsumoto, Hiroaki Yamato, Takaharu Taketomi, Takeshi Uchiumi, Fusanori Nishimura

    Archives of Oral Biology   83   241 - 251   2017.11

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    Objectives Amelogenin, the major component of the enamel matrix derivative (EMD), has been suggested as a bioactive candidate for periodontal regeneration. Apart from producing a regenerative effect on periodontal tissues, amelogenin has also been reported to have an anti-inflammatory effect. However, the precise molecular mechanisms underlying these effects remain unclear. In the present study, we examined the immunomodulatory effects of amelogenin on macrophages. Design Human phorbol 12-myristate 13-acetate (PMA)-differentiated U937 macrophages and CD14+ peripheral blood-derived monocytes (PBMC)-derived macrophages were stimulated with recombinant amelogenin (rM180). After performing a detailed microarray analysis, the effects of rM180 on macrophage phenotype and signal transduction pathways were evaluated by real-time polymerase chain reaction, enzyme-linked immunosorbent assay, confocal microscopy and flow cytometry. Results The microarray analysis demonstrated that rM180 increased the expression of anti-inflammatory genes in lipopolysaccharide (LPS)-challenged macrophages after 24 h, while it temporarily up-regulated inflammatory responses at 4 h. rM180 significantly enhanced the expression of M2 macrophage markers (CD163 and CD206). rM180-induced M2 macrophage polarisation was associated with morphological changes as well as vascular endothelial growth factor (VEGF) production. rM180 enhanced prostaglandin E2 (PGE2) expression, and the activation of the cAMP/cAMP-responsive element binding (CREB) signaling pathway was involved in amelogenin-induced M2 macrophage polarisation. Blocking of PGE2 signaling by indomethacin specifically abrogated rM180 with or without LPS-induced M2 shift in PBMC-derived macrophages. Conclusion Amelogenin could reprogram macrophages into the anti-inflammatory M2 phenotype. It could therefore contribute to the early resolution of inflammation in periodontal lesions and provide a suitable environment for remodeling-periodontal tissues.

    DOI: 10.1016/j.archoralbio.2017.08.005

  • Angiopoietin-like protein 2 is a positive regulator of osteoblast differentiation Reviewed

    Aiko Takano, Takao Fukuda, Takanori Shinjo, Misaki Iwashita, Etsuko Matsuzaki, Kensuke Yamamichi, Masaaki Takeshita, Terukazu Sanui, Fusanori Nishimura

    Metabolism: Clinical and Experimental   69   157 - 170   2017.4

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    Introduction and Aims Several studies have reported that angiopoietin-like protein 2 (Angptl2) is expressed abundantly in adipocytes and is associated with adipose tissue inflammation. In the present study, we found that osteoblasts and mesenchymal stem cells also expressed Angptl2 at high levels. The aim of this study was to understand the role of Angptl2 in osteoblastic cell differentiation. Methods Angptl2 expression was examined during osteoblast and adipocyte differentiation. The role of Angptl2 on cell differentiation and associated signaling was analyzed by gene knockdown using Angptl2 small interfering ribonucleic acid (siRNA). Results Angptl2 was highly expressed in MC3T3-E1 cells, ST2 cells and primary osteoblasts, but not in RAW264 cells. Inhibition of Angptl2 expression using siRNA markedly inhibited alkaline phosphatase (ALP) expression and osteoblastic differentiation in MC3T3-E1, ST2 cells and primary osteoblasts. Angptl2 siRNA also inhibited adipocyte differentiation in ST2 cells. Treatment of MC3T3-E1 cells with Angptl2 siRNA led to the down-regulation of the activities of several cell signaling pathways, including extracellular signal-regulated kinase (ERK), Jun amino-terminal kinase (JNK), Akt, and nuclear factor kappa B (NF-κB) signals. It also down-regulated the expression of Osterix, but not that of runt-related transcription factor 2 (Runx2), suggesting that Angptl2 is a positive activator of Osterix and its down-stream signals. Treatment of MC3T3-E1 cells with anti-Angptl2 antibodies suppressed ALP gene expression. In addition, treatment of Angptl2 siRNA-treated cells with culture supernatants of normal MC3T3-E1 cells restored ALP gene expression, indicating that Angptl2 acts in an autocrine manner. Conclusions The results suggest that Angptl2 is an autocrine positive regulator of cell differentiation. Thus, it is suggested that Angptl2 regulates not only adipose tissue metabolism but also bone metabolism.

    DOI: 10.1016/j.metabol.2017.01.006

  • Epicatechin downregulates adipose tissue CCL19 expression and thereby ameliorates diet-induced obesity and insulin resistance Reviewed

    Tomomi Sano, S. Nagayasu, S. Suzuki, Misaki Iwashita, Akiko Yamashita, T. Shinjo, Terukazu Sanui, A. Kushiyama, T. Kanematsu, T. Asano, Fusanori Nishimura

    Nutrition, Metabolism and Cardiovascular Diseases   27 ( 3 )   249 - 259   2017.3

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    Background and aims Epicatechin (EC) intake has been suggested to be beneficial for the prevention of cardiovascular disorders, and it is well known that adipose tissue inflammation is one of the major risk factors for coronary heart diseases. The purpose of the present study was to determine the in vitro and in vivo effects of EC on adipose tissue inflammation and obesity. Methods and results DNA microarray analysis was performed to evaluate the effects of EC on gene expression in adipocytes co-cultured with bacterial endotoxin-stimulated macrophages. To determine the in vivo effects of the catechin, C57BL/6 mice were fed either a high-fat diet (HFD) or HFD combined with EC, and metabolic changes were observed EC suppressed the expression of many inflammatory genes in the adipocytes co-cultured with endotoxin-stimulated macrophages. Specifically, EC markedly suppressed chemokine (C–C motif) ligand 19 (CCL19) expression. The target cell of EC appeared to macrophages. The in vivo study indicated that mice fed the EC-supplemented HFD were protected from diet-induced obesity and insulin resistance. Accordingly, the expression levels of genes associated with inflammation in adipose tissue and in the liver were downregulated in this group of mice. Conclusions EC exerts beneficial effects for the prevention of adipose tissue inflammation and insulin resistance. Since we previously reported that mice deficient in the CCL19 receptor were protected from diet-induced obesity and insulin resistance, it can be concluded that the beneficial effects of EC could be mediated, at least in part, by marked suppression of CCL19 expression.

    DOI: 10.1016/j.numecd.2016.11.008

  • The influence of periodontal burden on metabolic control of diabetes - Myth or reality? From a nutritional perspective - Invited Reviewed International journal

    Fusanori Nishimura, Tomomi Sano, Terukazu Sanui,

    Current Oral Health Reports   4   59 - 63   2017.3

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    DOI: doi:10.1007/s.40496-017-0136-0

  • Antibiotic effects against periodontal bacteria in organ cultured tissue Reviewed

    Masaaki Takeshita, Akira Haraguchi, Mayumi Miura, Takafumi Hamachi, Takao Fukuda, Terukazu Sanui, Aiko Takano, Fusanori Nishimura

    Clinical and Experimental Dental Research   3 ( 1 )   5 - 12   2017.2

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    Mechanical reduction of infectious bacteria by using physical instruments is considered the principal therapeutic strategy for periodontal disease; addition of antibiotics is adjunctive. However, local antibiotic treatment, combined with conventional mechanical debridement, has recently been shown to be more effective in periodontitis subjects with type 2 diabetes. This suggests that some bacteria may invade the inflamed inner gingival epithelium, and mechanical debridement alone will be unable to reduce these bacteria completely. Therefore, we tried to establish infected organ culture models that mimic the inner gingival epithelium and aimed to see the effects of antibiotics in these established models. Mouse dorsal skin epithelia were isolated, and periodontal bacteria were injected into the epithelia. Infected epithelia were incubated with test antibiotics, and colony-forming ability was evaluated. Results indicated that effective antibiotics differed according to injected bacteria and the bacterial combinations tested. Overall, in organ culture model, the combination of amoxicillin or cefdinir and metronidazole compensate for the effects of less effective bacterial combinations on each other. This in vitro study would suggest effective periodontal treatment regimens, especially for severe periodontitis.

    DOI: 10.1002/cre2.48

  • Innate immune-stimulatory activity of Porphyromonas gingivalis fimbriae is eliminated by phase separation using Triton X-114 Reviewed

    Kohji Nozoe, Terukazu Sanui, Masaaki Takeshita, Takao Fukuda, Akira Haraguchi, Yoshitomi Aida, Fusanori Nishimura

    Journal of Immunological Methods   441   31 - 38   2017.2

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    Fimbriae are virulence factors of Porphyromonas gingivalis (P. gingivalis). In this study, the action of fimbriae on neutrophil respiratory burst and cytokine production by mononuclear cells (MNC) were investigated. Native or denatured form of purified P. gingivalis fimbriae contained endotoxin at an equivalence of 1– 3 μg lipopolysaccharides (LPS)/mg protein. The endotoxin could be reduced to the equivalent of 1 ng-LPS/mg protein by phase separation using Triton X-114. Unfractionated fimbriae caused serum-dependent priming of neutrophils for enhanced respiratory burst, but both native and denatured forms of Triton X-114-fractionated fimbriae were not active at 100 μg/mL. Unfractionated fimbriae induced serum-dependent production of IL-1β by MNC. Triton X-114-fractionated fimbriae (10 μg/mL)-induced production of IL-1β, IL-8 or TNF-α was much lower than that induced by unfractionated fimbriae or 10 ng/mL P. gingivalis-LPS preparation. Triton X-114-fractionated fimbriae immobilized on polystyrene tubes induced adhesion-stimulated superoxide release by LPS-primed neutrophils in a β2 integrin-dependent manner. P. gingivalis cells caused priming of neutrophils; however, Toll-like receptor (TLR) 4 antagonists did not affect this response. Thus, P. gingivalis fimbriae were ineffective in inducing innate immune response in leukocytes; however, they induced β2 integrin-mediated response by neutrophils. Immune-stimulatory components of P. gingivalis might be recognized by receptors other than TLR4.

    DOI: 10.1016/j.jim.2016.11.012

  • Sprouty2 is involved in the control of osteoblast proliferation and differentiation through the FGF and BMP signaling pathways Reviewed

    Takaharu Taketomi, Tomohiro Onimura, Daigo Yoshiga, Daichi Muratsu, Terukazu Sanui, Takao Fukuda, Jingo Kusukawa, Seiji Nakamura

    Cell Biology International   2017.1

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    Fibroblast growth factor (FGF) and bone morphogenetic protein (BMP) play essential roles in bone formation and osteoblast activity through the extracellular signal-regulated kinase 1/2 (ERK1/2) and Smad pathways. Sprouty family members are intracellular inhibitors of the FGF signaling pathway, and four orthologs of Sprouty have been identified in mammals. In vivo analyses have revealed that Sprouty2 is associated with bone formation. However, the mechanism by which the Sprouty family controls bone formation has not been clarified. In this study, we investigated the involvement of Sprouty2 in osteoblast proliferation and differentiation. We examined Sprouty2 expression in MC3T3-E1 cells, and found that high levels of Sprouty2 expression were induced by basic FGF stimulation. Overexpression of Sprouty2 in MC3T3-E1 cells resulted in suppressed proliferation compared with control cells. Sprouty2 negatively regulated the phosphorylation of ERK1/2 after basic FGF stimulation, and of Smad1/5/8 after BMP stimulation. Furthermore, Sprouty2 suppressed the expression of osterix, alkaline phosphatase, and osteocalcin mRNA, which are markers of osteoblast differentiation. Additionally, Sprouty2 inhibited osteoblast matrix mineralization. These results suggest that Sprouty2 is involved in the control of osteoblast proliferation and differentiation by downregulating the FGF-ERK1/2 and BMP-Smad pathways, and suppresses the induction of markers of osteoblast differentiation.

    DOI: 10.1002/cbin.10876

  • IL-17A synergistically enhances TNFα-induced IL-6 and CCL20 production in 3T3-L1 adipocytes Reviewed

    Takanori Shinjo, Misaki Iwashita, Akiko Yamashita, Tomomi Sano, Mitsudai Tsuruta, Hiroaki Matsunaga, Terukazu Sanui, Tomoichiro Asano, Fusanori Nishimura

    Biochemical and Biophysical Research Communications   477 ( 2 )   241 - 246   2016.8

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    Interleukin-17A (IL-17A) is known to induce inflammatory responses and to be involved in the pathogenesis of not only autoimmune diseases, but also several metabolic and infectious diseases. In this study, IL-17A is shown to induce IL-6 expression in 3T3-L1 mature adipocytes. Interestingly, we found that IL-17A synergistically amplified TNFα-induced secretion of IL-6 and upregulation of IL-17RA expression in 3T3-L1 adipocytes. Its synergistic effects on IL-6 production were inhibited by pre-treatment with inhibitors of IκBα and JNK. Furthermore, IL-17A cooperatively enhanced LPS-mediated IL-6 production in 3T3-L1 adipocytes co-cultured with RAW264.7 macrophages. In addition, IL-17A also enhanced CCL20 production in 3T3-L1 adipocytes stimulated with TNFα or co-cultured with LPS-stimulated RAW macrophages. In high-fat diet-fed mouse epididymal adipose tissues, IL-17RA and RORγt mRNA levels were significantly increased and the serum level of CCL20 was also upregulated. Taken together, these data show that, in adipose tissues, IL-17A contributes to exacerbating insulin resistance-enhancing IL-6 production and promotes the infiltration of Th17 cells in cooperation with TNFα; these findings represent a novel hypothesis for the association between IL-17A-producing cells and type 2 diabetes.

    DOI: 10.1016/j.bbrc.2016.06.049

  • Mechanisms of the Macrolide-Induced Inhibition of Superoxide Generation by Neutrophils Reviewed

    Kohji Nozoe, Yoshitomi Aida, Takao Fukuda, Terukazu Sanui, Fusanori Nishimura

    Inflammation   39 ( 3 )   1039 - 1048   2016.6

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    The effect of macrolides on the superoxide (O2 ) production by neutrophils was studied. Resting neutrophils become primed by lipopolysaccharide (LPS) or N-formyl-methionyl-leucyl-phenylalanine (fMLP), and primed neutrophils generate O2 in response to fMLP or adhesion, respectively. Both LPS-primed fMLP-stimulated O2 generation by macrolide-treated neutrophils and adhesion-stimulated O2 generation by macrolide-treated fMLP-primed neutrophils were inhibited. Macrolide inhibition of O2 generation was dependent on serum or pH. Serum could be substituted by NaHCO3. The intensity of inhibition was azithromycin = roxithromycin > clarithromycin > erythromycin, in that order. Non-antimicrobial derivatives of erythromycin, that is, EM703 and EM900, inhibited O2 generation at pH 7.4. NH4Cl abolished the activity of azithromycin (AZ) only when added to neutrophils with AZ but not after incubation with AZ, suggesting that NH4Cl prevented the influx of AZ. AZ did not affect the expression of alkaline phosphatase, CD11b, and cytochrome b558 in both resting and LPS-primed neutrophils. These results suggested that macrolides did not affect granule mobilization but inhibited O2 generation selectively.

    DOI: 10.1007/s10753-016-0333-3

  • Disaggregation of lipopolysaccharide by albumin, hemoglobin or high-density lipoprotein, forming complexes that prime neutrophils for enhanced release of superoxide Reviewed

    Toshiya Komatsu, Yoshitomi Aida, Takao Fukuda, Terukazu Sanui, Shunji Hiratsuka, Michael J. Pabst, Fusanori Nishimura

    Pathogens and Disease   74 ( 3 )   2016.4

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    We studied the interaction of LPS with albumin, hemoglobin or high-density lipoprotein (HDL), and whether the interaction affected the activity of LPS on neutrophils. These proteins disaggregated LPS, depending upon temperature and LPS:protein ratio. Albumin-treated LPS was absorbed by immobilized anti-albumin antibody and was eluted with Triton X-100, indicating that LPS formed a hydrophobic complex with albumin. Rd mutant LPS was not disaggregated by the proteins, and did not form a complex with the proteins. But triethylamine-treated Rd mutant LPS formed complexes. When LPS was incubated with an equal concentration of albumin and with polymyxin B (PMXB), PMXB-LPS-protein three-way complexes were formed. After removal of PMXB, the complexes consisted of 11-15 LPS monomers bound to one albumin or hemoglobin molecule. LPS primed neutrophils for enhanced release of formyl peptide-stimulated superoxide, in a serum- and LPS-binding protein (LBP)-dependent manner. Although LPS plus LBP alone did not prime neutrophils, albumin-, hemoglobin- or HDL-treated LPS primed neutrophils when added with LBP. Triethylamine-treated Rd mutant LPS primed neutrophils only when incubated with one of the proteins and with LBP. Thus, in addition to LBP, disaggregation and complex formation of LPS with one of these proteins is required for LPS to prime neutrophils.

    DOI: 10.1093/femspd/ftw003

  • Inhibition of Sprouty2 polarizes macrophages toward an M2 phenotype by stimulation with interferon γ and Porphyromonas gingivalis lipopolysaccharide. Reviewed International journal

    後村 亮, 讃井 彰一, 福田 隆男, 田中 麗, 豊田 敬介, 山道 研介, 武富 孝治, 西村 英紀

    Immunity, Inflammation and Disease   26 ( 4 )   98 - 110   2016.2

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    DOI: 10.1002/iid3.99

  • Grp78 Is Critical for Amelogenin-Induced Cell Migration in a Multipotent Clonal Human Periodontal Ligament Cell Line Reviewed

    Kyousuke Toyoda, Takao Fukuda, Terukazu Sanui, Urara Tanaka, Kensuke Yamamichi, Ryo Atomura, Hidefumi Maeda, Atsushi Tomokiyo, Takaharu Taketomi, Takeshi Uchiumi, Fusanori Nishimura

    Journal of Cellular Physiology   231 ( 2 )   414 - 427   2016.1

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    Periodontal ligament stem cells (PDLSCs) are known to play a pivotal role in regenerating the periodontium. Amelogenin, which belongs to a family of extracellular matrix (ECM) proteins, is a potential bioactive molecule for periodontal regenerative therapy. However, its downstream target molecules and/or signaling patterns are still unknown. Our recent proteomic study identified glucose-regulated protein 78 (Grp78) as a new amelogenin-binding protein. In this study, we demonstrate, for the first time, the cellular responses induced by the biological interaction between amelogenin and Grp78 in the human undifferentiated PDL cell line 1-17, which possesses the most typical characteristics of PDLSCs. Confocal co-localization experiments revealed the internalization of recombinant amelogenin (rM180) via binding to cell surface Grp78, and the endocytosis was inhibited by the silencing of Grp78 in 1-17 cells. Microarray analysis indicated that rM180 and Grp78 regulate the expression profiles of cell migration-associated genes in 1-17 cells. Moreover, Grp78 overexpression enhanced rM180-induced cell migration and adhesion without affecting cell proliferation, while silencing of Grp78 diminished these activities. Finally, binding of rM180 to Grp78 promoted the formation of lamellipodia, and the simultaneous activation of Rac1 was also demonstrated by NSC23766, a widely accepted Rac1 inhibitor. These results suggest that Grp78 is essential for enhancing amelogenin-induced migration in 1-17 cells. The biological interaction of amelogenin with Grp78 offers significant therapeutic potential for understanding the biological components and specific functions involved in the signal transduction of amelogenin-induced periodontal tissue regeneration. J. Cell. Physiol. 231: 414-427, 2016.

    DOI: 10.1002/jcp.25087

  • Sprouty2 inhibition promotes proliferation and migration of periodontal ligament cells Reviewed

    Urara Tanaka, Terukazu Sanui, Takao Fukuda, Kyousuke Toyoda, T. Taketomi, R. Atomura, K. Yamamichi, Hidefumi Maeda, Fusanori Nishimura

    Oral Diseases   21 ( 8 )   977 - 986   2015.11

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    Objectives: We previously demonstrated that a dominant-negative Sprouty2 (Spry2) mutation promotes osteoblast proliferation and differentiation after basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF) stimulation, whereas it diminishes proliferation of gingival epithelial cells, thereby inducing favourable conditions for periodontal tissue regeneration. In this study, we investigated how Spry2 inhibition affects the cellular physiology of periodontal ligament (PDL) cells. Methods: A total of 1-17 PDL cells (multipotent clonal human PDL cell line) were stimulated with bFGF and EGF after transfection of Spry2 siRNA. Cell proliferation, migration, ALP staining, real-time PCR, Western blot and immunofluorescence assays were performed. Results: ERK1/2 activation and proliferation of 1-17 PDL cells were significantly upregulated by the addition of Spry2 siRNA in the presence of bFGF and EGF. In addition, Spry2 siRNA reduced transcription of osteogenesis-related genes and ALP staining relative to control cells. Furthermore, it increased AKT/phosphatidylinositol 3-kinase (PI3K) phosphorylation; consequently, Rac1 but not Cdc42 was activated, thereby promoting lamellipodia formation, cell proliferation and migration after stimulation by bFGF and EGF. Conclusion: Spry2 combined with bFGF and EGF stimulation reduced PDL cell migration and proliferation with inducing osteoblastic differentiation. These in vitro findings may provide a molecular basis for novel therapeutic approaches for establishing periodontal tissue regeneration.

    DOI: 10.1111/odi.12369

  • Identification of Novel Amelogenin-Binding Proteins by Proteomics Analysis Reviewed

    Takao Fukuda, Terukazu Sanui, Kyousuke Toyoda, Urara Tanaka, Takaharu Taketomi, Takeshi Uchiumi, Fusanori Nishimura

    PLoS One   8 ( 10 )   2013.10

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    Emdogain (enamel matrix derivative, EMD) is well recognized in periodontology. It is used in periodontal surgery to regenerate cementum, periodontal ligament, and alveolar bone. However, the precise molecular mechanisms underlying periodontal regeneration are still unclear. In this study, we investigated the proteins bound to amelogenin, which are suggested to play a pivotal role in promoting periodontal tissue regeneration. To identify new molecules that interact with amelogenin and are involved in osteoblast activation, we employed coupling affinity chromatography with proteomic analysis in fractionated SaOS-2 osteoblastic cell lysate. In SaOS-2 cells, many of the amelogenin-interacting proteins in the cytoplasm were mainly cytoskeletal proteins and several chaperone molecules of heat shock protein 70 (HSP70) family. On the other hand, the proteomic profiles of amelogenin-interacting proteins in the membrane fraction of the cell extracts were quite different from those of the cytosolic-fraction. They were mainly endoplasmic reticulum (ER)-associated proteins, with lesser quantities of mitochondrial proteins and nucleoprotein. Among the identified amelogenin-interacting proteins, we validated the biological interaction of amelogenin with glucose-regulated protein 78 (Grp78/Bip), which was identified in both cytosolic and membrane-enriched fractions. Confocal co-localization experiment strongly suggested that Grp78/Bip could be an amelogenin receptor candidate. Further biological evaluations were examined by Grp78/Bip knockdown analysis with and without amelogenin. Within the limits of the present study, the interaction of amelogenin with Grp78/Bip contributed to cell proliferation, rather than correlate with the osteogenic differentiation in SaOS-2 cells. Although the biological significance of other interactions are not yet explored, these findings suggest that the differential effects of amelogenin-derived osteoblast activation could be of potential clinical significance for understanding the cellular and molecular bases of amelogenin-induced periodontal tissue regeneration.

    DOI: 10.1371/journal.pone.0078129

  • Sprouty2 controls proliferation of palate mesenchymal cells via fibroblast growth factor signaling Reviewed

    Kaori Matsumura, Takaharu Taketomi, Keigo Yoshizaki, Shinsaku Arai, Terukazu Sanui, Daigo Yoshiga, Akihiko Yoshimura, Seiji Nakamura

    Biochemical and Biophysical Research Communications   404 ( 4 )   1076 - 1082   2011.1

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    Cleft palate is one of the most common craniofacial deformities. The fibroblast growth factor (FGF) plays a central role in reciprocal interactions between adjacent tissues during palatal development, and the FGF signaling pathway has been shown to be inhibited by members of the Sprouty protein family. In this study, we report the incidence of cleft palate, possibly caused by failure of palatal shelf elevation, in Sprouty2-deficient (KO) mice. Sprouty2-deficient palates fused completely in palatal organ culture. However, palate mesenchymal cell proliferation estimated by Ki-67 staining was increased in Sprouty2 KO mice compared with WT mice. Sprouty2-null palates expressed higher levels of FGF target genes, such as Msx1, Etv5, and Ptx1 than WT controls. Furthermore, proliferation and the extracellular signal-regulated kinase (Erk) activation in response to FGF was enhanced in palate mesenchymal cells transfected with Sprouty2 small interfering RNA. These results suggest that Sprouty2 regulates palate mesenchymal cell proliferation via FGF signaling and is involved in palatal shelf elevation.

    DOI: 10.1016/j.bbrc.2010.12.116

  • DOCK2 is required in T cell precursors for development of Vα14 NK T cells Reviewed

    Yuya Kunisaki, Yoshihiko Tanaka, Terukazu Sanui, Ayumi Inayoshi, Mayuko Noda, Toshinori Nakayama, Michishige Harada, Masaru Taniguchi, Takehiko Sasazuki, Yoshinori Fukui

    Journal of Immunology   176 ( 8 )   4640 - 4645   2006.4

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    Mouse CD1d-restricted Vα14 NKT cells are a unique subset of lymphocytes, which play important roles in immune regulation, tumor surveillance and host defense against pathogens. DOCK2, a mammalian homolog of Caenorhabditis elegans CED-5 and Drosophila melanogaster myoblast city, is critical for lymphocyte migration and regulates T cell responsiveness through immunological synapse formation, yet its role in Vα14 NKT cells remains unknown. We found that DOCK2 deficiency causes marked reduction of Vα14 NKT cells in the thymus, liver, and spleen. When α-galactesylceramide (α-GalCer), a ligand for Vα14 NKT cells, was administrated, cytokine production was scarcely detected in DOCK2-deficient mice, suggesting that DOCK2 deficiency primarily affects generation of Vα14 NKT cells. Supporting this idea, staining with CD1d/α-GalCer tetramers revealed that CD44 -NK1.1- Vα14 NKT cell precursors are severely reduced in the thymuses of DOCK2-deficient mice. In addition, studies using bone marrow chimeras indicated that development of Vα14 NKT cells requires DOCK2 expression in T cell precursors, but not in APCs. These results indicate that DOCK2 is required for positive selection of Vα14 NKT cells in a cell-autonomous manner, thereby suggesting that avidity-based selection also governs development of this unique subset of lymphocytes in the thymus.

  • Deletion of DOCK2, a regulator of the actin cytoskeleton in lymphocytes, suppresses cardiac allograft rejection Reviewed

    Hongsi Jiang, Fan Pan, Laurie M. Erickson, Mei Shiang Jang, Terukazu Sanui, Yuya Kunisaki, Takehiko Sasazuki, Masakazu Kobayashi, Yoshinori Fukui

    Journal of Experimental Medicine   202 ( 8 )   1121 - 1130   2005.10

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    Allograft rejection is induced by graft tissue infiltration of alloreactive T cells that are activated mainly in secondary lymphoid organs of the host. DOCK2 plays a critical role in lymphocyte homing and immunological synapse formation by regulating the actin cytoskeleton, yet its role in the in vivo immune response remains unknown. We show here that DOCK2 deficiency enables long-term survival of cardiac allografts across a complete mismatch of the major histocompatibility complex molecules. In DOCK2-deficient mice, alloreactivity and allocytotoxicity were suppressed significantly even after in vivo priming with alloantigens, which resulted in reduced intragraft expression of effector molecules, such as interferon-γ, granzyme B, and perforin. This is mediated, at least in part, by preventing potentially alloreactive T cells from recruiting into secondary lymphoid organs. In addition, we found that DOCK2 is critical for CD28-mediated Rac activation and is required for the full activation of alloreactive T cells. Although DOCK2-deficient, alloreactive T cells were activated in vitro in the presence of exogenous interleukin-2, these T cells, when transferred adoptively, failed to infiltrate into the allografts that were transplanted into RAG1-deficient mice. Thus, DOCK2 deficiency attenuates allograft rejection by simultaneously suppressing multiple and key processes. We propose that DOCK2 could be a novel molecular target for controlling transplant rejection. JEM

    DOI: 10.1084/jem.20050911

  • Defective fetal liver erythropoiesis and T lymphopoiesis in mice lacking the phosphatidylserine receptor Reviewed

    Yuya Kunisaki, Sadahiko Masuko, Mayuko Noda, Ayumi Inayoshi, Terukazu Sanui, Mine Harada, Takehiko Sasazuki, Yoshinori Fukui

    Blood   103 ( 9 )   3362 - 3364   2004.5

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    Clearance of apoptotic cells by macrophages is considered important for prevention of inflammatory responses leading to tissue damage. The phosphatidylserine receptor (PSR), which specifically binds to phosphatidylserine (PS) exposed on the surface of apoptotic cells, mediates uptake of apoptotic cells in vitro, yet the physiologic relevance of PSR remains unknown. This issue was addressed by generating PSR-deficient (PSR -/-) mice. PSR-/- mice exhibited severe anemia and died during the perinatal period. In the PSR-/- fetal livers, erythroid differentiation was blocked at an early erythroblast stage. In addition, PSR-/- embryos exhibited thymus atrophy owing to a developmental defect of T-lymphoid cells. Clearance of apoptotic cells by macrophages was impaired in both liver and thymus of PSR-/- embryos. However, this did not induce up-regulation of inflammatory cytokines. These results indicate that during embryonic development, PSR-mediated apoptotic cell uptake is required for definitive erythropoiesis and T lymphopoiesis, independently of the prevention of inflammatory responses.

    DOI: 10.1182/blood-2003-09-3245

  • Organ-specific autoimmunity in mice whose T cell repertoire is shaped by a single antigenic peptide Reviewed

    T. Oono, Yoshinori Fukui, S. Masuko, O. Hashimoto, T. Ueno, Terukazu Sanui, A. Inayoshi, Mami Noda, M. Sata, T. Sasazuki

    Journal of Clinical Investigation   108 ( 11 )   1589 - 1596   2001.12

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    Organ-specific autoimmune diseases have been postulated to be the result of T cell response against organ-specific self-peptides bound to MHC molecules. Contrary to this paradigm, we report here that transgenic mice lacking MHC class I expression and expressing an MHC class II I-Ab molecule that presents only a single peptide (Eα52-68) spontaneously develops peripheral nervous system-specific autoimmune disease with many of the histopathological features found in experimental allergic neuritis. Reciprocal bone marrow chimeras produced using susceptible and resistant lines revealed that bone marrow-derived cells determined disease susceptibility. While the expression of the I-Ab-Eα52-68 complex in the periphery was readily detectable in both lines, its expression on thymic dendritic cells responsible for tolerance induction was markedly lower in the susceptible line than in the resistant line. Consistent with this, CD4+ T cells that can be activated by the I-Ab-Eα52-68 complex were found in the susceptible line, but not in the resistant line. Such CD4+ T cells conferred the disease to the resistant line by adoptive transfer, and administration of Ab specific for the I-Ab-Eα52-68 complex inhibited disease manifestation in the susceptible line. These results indicate that disease development involves systemic T cell reactivity to I-Ab-Eα52-68 complex, probably caused by incomplete negative thymocyte selection.

    DOI: 10.1172/JCI200113256

  • Haematopoietic cell-specific CDM family protein DOCK2 is essential for lymphocyte migration Reviewed

    Yoshinori Fukui, Osamu Hashimoto, Terukazu Sanui, Takamasa Oono, Hironori Koga, Masaaki Abe, Ayumi Inayoshi, Mayuko Noda, Masahiro Oike, Toshikazu Shirai, Takehiko Sasazuki

    Nature   412 ( 6849 )   826 - 831   2001.8

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    Cell migration is a fundamental biological process involving membrane polarization and cytoskeletal dynamics, both of which are regulated by Rho family GTPases. Among these molecules, Rac is crucial for generating the actin-rich lamellipodial protrusion, a principal part of the driving force for movement. The CDM family proteins, Caenorhabditis elegans CED-5, human DOCK180 and Drosophila melanogaster Myoblast City (MBC), are implicated to mediate membrane extension by functioning upstream of Rac. Although genetic analysis has shown that CED-5 and Myoblast City are crucial for migration of particular types of cells, physiological relevance of the CDM family proteins in mammals remains unknown. Here we show that DOCK2, a haematopoietic cell-specific CDM family protein, is indispensable for lymphocyte chemotaxis. DOCK2-deficient mice (DOCK2-/-) exhibited migration defects of T and B lymphocytes, but not of monocytes, in response to chemokines, resulting in several abnormalities including T lymphocytopenia, atrophy of lymphoid follicles and loss of marginal-zone B cells. In DOCK2-/- lymphocytes, chemokine-induced Rac activation and actin poly- merization were almost totally abolished. Thus, in lymphocyte migration DOCK2 functions as a central regulator that mediates cytoskeletal reorganization through Rac activation.

    DOI: 10.1038/35090591

  • Diversity of T cell repertoire shaped by a single peptide ligand is critically affected by its acid residue at a T cell receptor contact Reviewed

    Yoshinori Fukui, Takamasa Oono, Jean Pierre Cabaniols, Kazuki Nakao, Katsuiku Hirokawa, Ayumi Inayoshi, Terukazu Sanui, Jean Kanellopoulos, Eiko Iwata, Mayuko Noda, Motoya Katsuki, Philippe Kourilsky, Takehiko Sasazuki

    Proceedings of the National Academy of Sciences of the United States of America   97 ( 25 )   13760 - 13765   2000.12

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    T cell differentiation in the thymus is driven by positive selection through the interaction of αβ T cell receptors (TCRs) with selfpeptides bound to self-major histocompatibility complex molecules, yet the influence of the peptide sequence on this process remains unknown. To address this issue, we have compared CD4+ T cell differentiation between two sets of mouse lines in which MHC class II I-Ab molecules are occupied with either Eα chain-derived peptide (pEα) or its variant, (p)60k, with one amino acid substitution from leucine to lysine at P5 residue of TCR contacts. Here, we show that despite the comparable expression of I-Ab-peptide complex in the thymus, this substitution from leucine to lysine affects efficiency of positive selection, resulting in extremely small numbers of CD4+ T cells to be selected to mature on I-Ab-(p)60k complex. Furthermore, we show that, although I-Ab-pEα complex selects diverse T cells, T cell repertoire shaped by I-Ab-(p)60k complex is markedly constrained. Our findings thus suggest that positive selection is both specific and degenerate, depending on the amino acid residues at TCR contacts of the selecting self-peptides.

    DOI: 10.1073/pnas.250470797

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Books

  • ザ・ペリオドントロジー第4版 第4章 歯周病の検査、診断と治療 2.歯周病の検査

    讃井彰一(Role:Joint author)

    永末書店  2023.2 

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    Responsible for pages:p99-102   Language:Japanese   Book type:Scholarly book

  • ミニレビュー 組織再生を目的としたアメロジェニン研究の現在

    讃井彰一、西村英紀(Role:Sole author)

    日本歯周病学会誌  2019.8 

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    Responsible for pages:p100-102   Language:Japanese   Book type:Scholarly book

  • 第4章 歯周病の検査・診断と治療 ザ・ペリオドントロジー 第3版2019.2.20

    讃井彰一(Role:Joint author)

    永末書店  2019.2 

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    Responsible for pages:p100-102   Language:Japanese   Book type:Scholarly book

  • 「bFGFシグナルのアンタゴニストを標的とした歯周組織再生療法の開発」 歯界展望 特別号2013

    讃井 彰一, 田中麗, 豊田敬介, 福田隆男, 後村亮, 濱地 貴文, 前田 勝正(Role:Joint author)

    医歯薬出版株式会社  2013.5 

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    Language:Japanese   Book type:Scholarly book

  • 「医局紹介:研究プロジェクトの精鋭たち/わが医局のエース」

    讃井彰一、前田勝正(Role:Joint author)

    2011.5 

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    Responsible for pages:ザ・クインテッセンス;30 (5), 200-201   Language:Japanese   Book type:General book, introductory book for general audience

  • DOCK2によるT細胞機能の制御 :臨床免疫

    讃井彰一,福井宣規(Role:Joint author)

    科学評論社  2004.3 

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    Responsible for pages:41巻3号,243-247頁   Language:Japanese   Book type:General book, introductory book for general audience

  • CDMファミリー分子DOCK2による免疫シナプス形成の制御 :細胞工学

    讃井彰一,福井宣規(Role:Joint author)

    秀潤社  2003.8 

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    Responsible for pages:22巻11号,1204-1207頁   Language:Japanese   Book type:General book, introductory book for general audience

  • 免疫応答におけるリンパ球の動態-HCH欠損マウスの情報-.:感染・炎症・免疫

    讃井彰一,福井宣規(Role:Joint author)

    2003.3 

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    Responsible for pages:医薬の門社   Language:Japanese   Book type:General book, introductory book for general audience

  • CDMファミリー分子DOCK2によるリンパ球遊走の制御.:メディカル・サイエンス・ダイジェスト臨時増刊号

    讃井彰一,福井宣規,笹月健彦(Role:Joint author)

    ニューサイエンス社  2002.4 

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    Responsible for pages:33巻1号,52-54頁   Language:Japanese   Book type:General book, introductory book for general audience

  • 日本歯周病学会編 糖尿病患者に対する歯周治療ガイドライン改定第3版

    西村英紀, 青山典生, 稲垣幸司, 梅﨑陽二朗, 讃井彰一, 白方良典, 鈴木茂樹, 高橋慶壮, 富田幸代, 内藤徹, 中川種昭, 長澤敏行, 中島貴子, 二宮雅美, 沼部幸博, 林丈一朗, 水谷幸嗣, 水野智仁, 三辺正人, 山下明子, 山本直史.(Role:Joint author)

    医歯薬出版株式会社  2023.6 

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    Responsible for pages:p102-106   Language:Japanese   Book type:Scholarly book

  • 「Y-box結合タンパク質の骨芽細胞における動態解析」 歯界展望 特別号2013

    福田隆男, 田中麗, 豊田敬介, 讃井 彰一, 武富 孝治, 後村亮, 濱地 貴文, 前田 勝正, 西村 英紀(Role:Joint author)

    医歯薬出版株式会社  2013.5 

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    Language:Japanese   Book type:Scholarly book

  • 「歯周組織細胞群における新規アメロジェニン結合タンパク質のプロテオーム解析」 歯界展望 特別号2013

    田中麗, 豊田敬介, 福田隆男, 讃井 彰一, 後村亮, 濱地 貴文, 前田 勝正(Role:Joint author)

    医歯薬出版株式会社  2013.5 

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    Language:Japanese   Book type:Scholarly book

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Presentations

  • 細胞骨格制御分子を標的とした新規歯周治療法の開発に関する基礎的研究 Invited

    讃井彰一

    第61回春季日本歯周病学会学術大会  2018.6 

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    Event date: 2018.6

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:京王プラザホテル、東京都   Country:Japan  

    細胞骨格制御分子を標的とした新規歯周治療法の開発に関する基礎的研究

  • 限局性侵襲性歯周炎患者にエナメルマトリックスデリバティブによる歯周組織再生療法を行った一症例

    讃井彰一,四本かれん,豊田敬介,福田隆男,田中麗,山道研介,西村英紀

    第60回春季日本歯周病学会学術大会  2017.5 

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    Event date: 2017.5

    Language:Japanese  

    Venue:福岡国際会館、福岡市   Country:Japan  

  • Spry2 Downregulation Shifts Macrophages Toward an M2 Phenotype by Stimulation with Interferon γ and Porphyromonas gingivalis Lipopolysaccharide. International conference

    Terukazu Sanui, Hajime Akiyama, Takao Fukuda, Urara Tanaka, Kyosuke Toyoda, Takaharu Taketomi, Fusanori Nishimura

    94th General Session & Exhibition of the International Association for Dental Research  2016.6 

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    Event date: 2016.6 - 2018.6

    Language:English  

    Venue:Seoul, South Korea   Country:Japan  

  • Spry2 Downregulation Shifts Macrophages Toward an M2 Phenotype by Stimulation with Interferon γ and Porphyromonas Gingivalis Lipopolysaccharide. International conference

    讃井 彰一, 福田隆男, 田中麗, 豊田敬介, 山道研介, 西村 英紀

    94rd General Session & Exhibition of the International Association for Dental Research  2016.6 

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    Event date: 2016.6

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Seoul   Country:Korea, Republic of  

  • Symposium 1: Spry2 is a new therapeutic target for periodontal tissue regeneration. International conference

    讃井 彰一

    The 63rd Annual Meeting of Japanese Association for Dental Research  2015.10 

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    Event date: 2015.10

    Language:English   Presentation type:Oral presentation (general)  

    Venue:福岡国際会議場   Country:Japan  

  • The Effects of Spry2 in Osteoblasts and Gingival Epithelial Cells. International conference

    讃井 彰一, 田中麗, 豊田敬介, 福田隆男, 後村亮, 山道研介, 西村 英紀

    93rd General Session & Exhibition of the International Association for Dental Research  2015.3 

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    Event date: 2015.3

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Haynes Convention Center, Boston   Country:United States  

  • Sprouty2 regulates cell proliferation and migration in periodontal ligament cells International conference

    田中麗, 讃井 彰一, 豊田敬介, 福田隆男, 後村亮, 山道研介, 西村 英紀

    93rd General Session & Exhibition of the International Association for Dental Research  2015.3 

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    Event date: 2015.3

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Haynes Convention Center, Boston   Country:United States  

  • Tyrosine 55 Mutation of Spry2 Induces Proliferation and Differentiation of Osteoblasts through bFGF and EGF Stimulation but Inhibits Proliferation of Gingival Epithelial Cells: Implications for Novel Biological Approach to Periodontal Regeneration.

    讃井 彰一, 豊田敬介, 福田隆男, 後村亮, 山道研介, 田中麗, 西村 英紀

    62nd Annual Meeting of Japanese Association for Dental Research  2014.12 

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    Event date: 2014.12

    Language:English   Presentation type:Oral presentation (general)  

    Venue:KKRホテル大阪、大阪市   Country:Japan  

  • 根分岐部病変を伴う慢性歯周炎患者に対し歯根分離および自然挺出にて対応した一症例

    讃井 彰一, 田中麗, 豊田敬介, 福田隆男, 後村亮, 山道研介, 西村 英紀

    第56回 秋季日本歯周病学会学術大会  2013.9 

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    Event date: 2013.9

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:前橋市   Country:Japan  

  • Inhibition of Spry2 decreased EGF receptors in gingival epithelial cells. International conference

    讃井 彰一, 田中麗, 豊田敬介, 福田隆男, 後村亮, 山道研介, 西村 英紀

    10th Asian Pacific Society of Periodontology Meeting  2013.9 

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    Event date: 2013.9

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Nara   Country:Japan  

  • Sprouty2 regulates degradation of EGF receptors in gingival epithelial cells. International conference

    讃井 彰一, 田中麗, 豊田敬介, 福田隆男, 武富孝治, 後村亮, 西村 英紀

    2nd meeting of IADR-APR  2013.8 

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    Event date: 2013.8

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Plaza Athenee, Bangkok   Country:Thailand  

  • Sprouty2 regulates osteoblastogenesis via Runx2 signaling. International conference

    Sanui Terukazu, Tanaka Urara, Toyoda Kyosuke, Fukuda Takao, Takaharu Taketomi, Atomura Ryo, Hamachi Takafumi, Maeda Katsumasa

    91nd General Session & Exhibition of the IADR  2013.3 

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    Event date: 2013.3

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Washington States Convention Center   Country:United States  

  • Inhibition of Sprouty2 Polarizes Macrophages toward M2 Phenotype in Periodontitis Invited International conference

    Terukazu Sanui, Urara Tanaka, Kyosuke Toyoda, Takao Fukuda, Ryo Atomura, Takafumi Hamachi, and Katsumasa Maeda

    Kyudai Oral Bioscience 2013 —7th International Symposium —  2013.3 

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    Event date: 2013.3

    Presentation type:Symposium, workshop panel (public)  

    Venue:Fukuoka Recent Hotel   Country:Japan  

    Periodontal disease is a chronic inflammatory response to bacterial pathogens involving the supporting tissues of the teeth. The anerobic bacterium, Porphyromonas gingivalis, has been implicated as a major etiologic agent in the development and progression of periodontitis. Lipopolysaccharide (LPS) from P. gingivalis induces pro-inflammatory cytokines in host macrophages. Macrophages can acquire distinct functional phenotypes, referred to as classically activated, pro-inflammatory macrophages (M1) and alternatively activated, anti-inflammatory macrophages (M2). M2 macrophages are associated with homeostatic functions linked to wound healing and tissue repair. Therefore, the inhibition of pro-inflammatory cytokine production in macrophages is the important biological reaction for the homeostasis after elimination of the etiologic agent.
    Sprouty proteins are identified as inhibitors of fibroblast growth factor (FGF) receptor. Specifically Sprouty2 (Spry2) functions as a negative regulator of receptor tyrosine kinases (RTKs) signaling, and is expressed in several developing organs including kidney, lung, brain, heart, skeletal muscle and craniofacial area. Furthermore, Spry2 has conserved function to modulate morphogenesis in several tissues. Recently, we demonstrated that inhibition of Spry2 induced cell proliferation and differentiation of MC3T3-E1osteoblastic cells, while it diminished cell proliferation of GE1gingival
    epithelial cells in vitro.
    We report here that suppression of Spry2 polarizes J774 mouse macrophages toward alternative macrophage activation (M2) phenotype when J774 cells are stimulated with LPS from P. gingivalis.
    This polarization is defined by surface protein expression, cytokine production and arginase activity. These data provide evidence that Spry2 inhibitors affect the inflammatory process at the level of the
    macrophage and shifts macrophage polarization from pro-inflammatory properties toward anti-inflammatory ones in periodontitis.
    Additionally, we are confirming how this response affects the periodontal tissue regeneration or the para-inflammation of periodontitis.

  • bFGFシグナルのアンタゴニストを標的とした歯周組織再生療法の開発

    讃井彰一、田中麗、福田隆男、豊田敬介、後村亮、濱地貴文、前田勝正

    第22 回日本歯科医学会総会  2012.11 

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    Event date: 2012.11

    Venue:大阪国際会議場   Country:Japan  

  • YB-1 regulates cell proliferation and differentiation in osteoblasts. International conference

    Terukazu Sanui, Kyosuke Toyoda, Takao Fukuda, Urara Tanaka, Ryou Atomura, Takafumi Hamachi, Katsumasa Maeda

    98th Annual Meeting American Academy of Periodontology in collaboration with the Japanese Society of Periodontology  2012.9 

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    Event date: 2012.10 - 2012.9

    Venue:Los Angels Convention Center   Country:United States  

  • Periodontal Regenerative Effect by Inhibition of Sprouty2 Protein. International conference

    T. SANUI, U. TANAKA, T. FUKUDA, K. TOYODA, T. TAKETOMI, R. ATOMURA, T. HAMACHI, and K. MAEDA

    Pan Europe Region / International Association for Dental Research (PER/IADR)Meeting  2012.9 

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    Event date: 2012.9

    Venue:Finlandia Hall   Country:Finland  

  • Suppression of Sprouty2 Induces Periodontal Tissue Regeneration. International conference

    T. SANUI, T. FUKUDA, T. TAKETOMI, T. HAMACHI, and K. MAEDA

    The 88th International Association for Dental Research (IADR)  2010.7 

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    Event date: 2010.7

    Presentation type:Oral presentation (general)  

    Venue:Center Conventions International Barcelona (CCIB)   Country:Spain  

  • Analysis of Streptococcus mutans Biofilm Proteins Recognized by Salivary IgA. International conference

    Terukazu Sanui and Richard L. Gregory

    The 87th International Association for Dental Research (IADR)  2009.4 

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    Event date: 2009.4

    Venue:Miami Beach Convention Center   Country:United States  

    Analysis of Streptococcus mutans Biofilm Proteins Recognized by Salivary IgA.

  • Tリンパ球の細胞高次機能制御におけるCDMファミリー分子DOCK2の役割

    讃井彰一、笹月健彦、福井宣規

    日本免疫学会  2002.12 

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    Presentation type:Oral presentation (general)  

    Venue:第32回日本免疫学会総会・学術集会 東京   Country:Japan  

  • 高親和性科可溶性TCRの樹立とその未知抗原ペプチド同定への応用

    讃井彰一、福井宣規、大野隆真、笹月健彦

    日本免疫学会  2000.11 

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    Venue:第30回日本免疫学会総会・学術集会 仙台   Country:Japan  

  • リンパ球の運動性を制御する分子の同定

    讃井彰一、福井宣規、橋本修、白井俊一、笹月健彦

    日本免疫学会  2001.12 

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    Presentation type:Oral presentation (general)  

    Country:Japan  

  • Endothelial insulin resistance contributes to the pathogenesis of diabetes-related periodontitis. International conference

    Chikako Hayashi, Masaaki Toyoda, Kentaro Kawakami, Yuki Nakao, Miyu Shida, Takanori Shinjo, Terukazu Sanui, Takao Fukuda, Fusanori Nishimura

    2024 IADR/AADOCR/CADR General Session & Exhibition  2024.3 

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    Event date: 2024.3

    Language:English  

    Venue:New Orleans   Country:United States  

  • Fabrication of Gingiva-Derived Stem Cell-Based Scaffold-Free Bone-Like 3D Structures International conference

    Masaaki Toyoda, Shunichi Kajioka, Takao Fukuda, Kentaro Kawakami, Miyu Shida, Chikako Hayashi, Tsukasa Aoki, Tatsuro Zeze, Yuki Nakao, Terukazu Sanui, Fusanori Nishimura

    2024 IADR/AADOCR/CADR General Session & Exhibition  2024.3 

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    Event date: 2024.3

    Language:English  

    Venue:New Orleans   Country:United States  

  • ヒト歯肉由来幹細胞を用いて作製した骨様立方構造体の解析.

    豊田真顕、梶岡俊一、福田隆男、藤本亮太、川上賢太郎、信太実有、李金鳳、林千華子、中尾雄紀、讃井彰一、中山功一、西村英紀

    第66回秋季日本歯周病学会学術大会  2023.12 

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    Event date: 2023.12

    Language:Japanese  

    Venue:アバンセホール、 佐賀市   Country:Japan  

  • バイオ3Dプリンターを用いた歯肉幹細胞由来骨様立体構造物の作製方法の確立と骨分化能、石灰化度に関する解析.

    豊田真顕、梶岡俊一、福田隆男、川上賢太郎、信太実有、李金鳳、林千華子、中尾雄紀、讃井彰一、西村英紀

    第66回秋季日本歯周病学会学術大会  2023.10 

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    Event date: 2023.10

    Language:Japanese  

    Venue:出島メッセ長崎、 長崎市   Country:Japan  

  • miR-582-5p, that targets Skp1 and suppresses NF-kB signaling-mediated inflammation, is down-regulated in periodontitis and obesity.

    Li Rongzhi, Tomomi Sano, Takao Fukuda, Takanori Shinjyo, Misaki Iwashita, Akiko Yamashita, Terukazu Sanui, Fusanori Nishimura.

    2023年度日本歯科保存学会春季学術大会(第158回)  2023.6 

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    Event date: 2023.6

    Language:Japanese  

    Venue:くにびきメッセ、松江市、島根県   Country:Japan  

  • バイオ3Dプリンターを用いた、間葉系幹細胞からの骨様立法構造物作製への挑戦

    豊田真顕、梶岡俊一、川上賢太郎、林千華子、渡邊ゆかり、中尾雄紀、四本かれん、讃井彰一、福田隆男、西村英紀

    令和4年度日本歯周病学会九州五大学 日本臨床歯周病学会九州支部合同研究会  2022.11 

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    Event date: 2022.11

    Language:Japanese  

    Venue:Web開催   Country:Japan  

  • ヒト歯髄細胞由来マイクロベジクル含有PKRを標的とした歯髄鎮静薬および歯内・歯周病変モデルの作成に向けて

    川上賢太郎、渡邊ゆかり、林千華子、豊田真顕、新城尊徳、讃井彰一、福田隆男、西村英紀

    令和4年度日本歯周病学会九州五大学 日本臨床歯周病学会九州支部合同研究会  2022.11 

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    Event date: 2022.11

    Language:Japanese  

    Venue:Web開催   Country:Japan  

  • Endothelial insulin resistance contributes to the exacerbation of diabetes-related periodontitis. International conference

    Tatsuro Zeze, Takanori Shinjo, Kohei Sato, Mio Imagawa, Yuki Nishimura, Misaki Iwashita, Takao Fukuda, Terukazu Sanui, Fusanori Nishimura.

    The 108th Annual Meeting of the American Academy of Periodontology  2022.10 

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    Event date: 2022.10

    Language:English  

    Venue:Phoenix, AZ   Country:United States  

  • Fabrication of stem cell-based scaffold-free bone-like 3D structures. International conference

    Toyoda M, Kajioka S, Fujimoto R, Hayashi C, Kawakami K, Watanabe Y, Nakao Y, Yotsumoto K, Sanui T, Fukuda T, Nakayama K, Nishimura. F.

    The 108th Annual Meeting of the American Academy of Periodontology  2022.10 

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    Event date: 2022.10

    Language:English  

    Venue:Phoenix, AZ   Country:United States  

  • miR-1260b inhibits periodontal bone loss by targeting ATF6β. International conference

    Hayashi C, Kawakami K, Toyoda M, Watanabe Y, Nakao Y, Yotsumoto K, Yamato H, Shinjo T, Sanui T, Fukuda T, Nishimura F.

    The 108th Annual Meeting of the American Academy of Periodontology  2022.10 

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    Event date: 2022.10

    Language:English  

    Venue:Phoenix, AZ   Country:United States  

  • Endothelial insulin resistance contributes to the pathogenesis of diabetes-related periodontitis. International conference

    Tatsuro Zeze, Takanori Shinjo, Kohei Sato, Mio Imagawa, Yuki Nishimura, Misaki Iwashita, Akiko Yamashita, Takao Fukuda, Terukazu Sanui, Fusanori Nishimura.

    2022 IADR/APR General Session & Exhibition  2022.6 

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    Event date: 2022.6

    Language:English  

    Venue:WEB開催   Country:China  

  • TNF-a/IFN-a共刺激した歯肉幹細胞由来エクソソームはCD73とCD5Lを介して抗炎症性M2マクロファージを誘導する

    渡邊ゆかり、林千華子、川上賢太郎、豊田真顕、中尾雄紀、大和寛明、四本かれん、新城尊徳、岩下未咲、讃井彰一、福田隆男、西村英紀

    2022年度日本歯科保存学会春季学術大会(第156回)  2022.6 

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    Event date: 2022.6

    Language:Japanese  

    Venue:Web開催   Country:Japan  

  • ヒト歯髄細胞由来マイクロベジクル含有PKRを標的とした歯髄鎮静薬および歯内・歯周病変モデルの作成に向けて

    川上賢太郎、渡邊ゆかり、林千華子、豊田真顕、新城尊徳、讃井彰一、福田隆男、西村英紀

    2022年度日本歯科保存学会春季学術大会(第156回)  2022.6 

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    Event date: 2022.6

    Language:Japanese  

    Venue:Web開催   Country:Japan  

  • バイオ3Dプリンターを用いた、間葉系幹細胞からの骨様立法構造物作製への挑戦

    豊田真顕、梶岡俊一、福田隆男、渡辺ゆかり、林千華子、川上賢太郎、中尾雄紀、四本かれん、大和寛明、讃井彰一、西村英紀

    第65回春季日本歯周病学会学術大会  2022.6 

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    Event date: 2022.6

    Language:Japanese  

    Venue:東京京王プラザホテル   Country:Japan  

  • 歯肉幹細胞由来エクソソーム内包miR-1260bによる小胞体ストレス応答制御を介した歯周炎骨吸収抑制効果

    林千華子、福田隆男、渡邊ゆかり、川上賢太郎、豊田真顕、中尾雄紀、四本かれん、大和寛明、新城尊徳、讃井彰一、西村英紀

    第65回春季日本歯周病学会学術大会  2022.6 

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    Event date: 2022.6

    Language:Japanese  

    Venue:東京京王プラザホテル   Country:Japan  

  • Exosomes from TNF-α-treated human gingiva-derived MSCs enhance M2 macrophage polarization and inhibit periodontal bone loss. International conference

    Yuki Nakao, Yukari Watanabe, Chikako Hayashi, Hiroaki Yamato, Karen Yotsumoto, Terukazu Sanui, Takanori Shinjo, Takao Fukuda, Fusanori Nishimura.

    Kyudai Oral Bioscience & OBT Research Center 5th Joint International Symposium  2021.11 

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    Event date: 2021.11

    Language:English  

    Venue:九州大学歯学部   Country:Japan  

  • Exosomal miR-1260b derived from TNF-α-treated hGMSCs inhibits periodontal bone loss by targeting ATF6β-mediated regulation of ER stress. International conference

    Chikako Hayashi, Takao Fukuda, Yukari Watanabe, Kentaro Kawakami, Masaaki Toyoda, Yuki Nakao, Karen Yotsumoto, Hiroaki Yamato, Takanori Shinjo, Terukazu Sanui, Fusanori Nishimura

    Kyudai Oral Bioscience & OBT Research Center 5th Joint International Symposium  2021.11 

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    Event date: 2021.11

    Language:English  

    Venue:九州大学歯学部   Country:Japan  

  • 肉幹細胞由来エクソソーム内包miR-1260bによる小胞体ストレス応答制御を介した歯槽骨吸収抑制作用.

    林千華子, 福田隆男, 渡邊ゆかり, 川上賢太郎, 豊田真顕, 中尾雄紀, 四本かれん, 大和寛明,新城尊徳,讃井彰一,西村英紀.

    2021年度日本歯科保存学会秋季学術大会(第155回)  2021.10 

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    Event date: 2021.10 - 2021.11

    Language:Japanese  

    Venue:Web開催   Country:Japan  

  • Exosomal miR-1260b derived from TNF-α-treated hGMSCs inhibits periodontal bone loss by targeting ATF6β-mediated regulation of ER stress. International conference

    Chikako Hayashi, Takao Fukuda, Yukari Watanabe, Kentaro Kawakami, Masaaki Toyoda, Yuki Nakao, Karen Yotsumoto, Hiroaki Yamato, Takanori Shinjo, Terukazu Sanui, Fusanori Nishimura.

    JADR 69th annual meeting  2021.10 

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    Event date: 2021.10

    Language:English  

    Venue:九州大学医学部百年講堂   Country:Japan  

  • High-fat diet-induced XAF1 exacerbates diabetes by promoting pancreatic β-cell apoptosis. International conference

    Yuki Nishimura, Misaki Iwashita, Masato Hayashi, Takanori Shinjo, Tatsuro Zeze, Akiko Yamashita, Takao Fukuda, Terukazu Sanui, Tomomi Sano, Fusanori Nishimura.

    JADR 69th annual meeting  2021.10 

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    Event date: 2021.10

    Language:English  

    Venue:九州大学医学部百年講堂   Country:Japan  

  • Exosomes derived from GMSCs stimulated with TNF-α and IFN-α promote M2 macrophage polarization via enhanced CD73 and CD5L expression. International conference

    Yukari Watanabe, Chikako Hayashi, Kentarou Kawakami, Masaaki Toyoda, Yuki Nakao, Karen Yotsumoto, Hiroaki Yamato, Takanori Shinjyo, Terukazu Sanui, Takao Fukuda, Fusanori Nishimura

    JADR 69th annual meeting  2021.10 

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    Event date: 2021.10

    Language:English  

    Venue:九州大学医学部百年講堂   Country:Japan  

  • ゲラニルゲラニルアセトンとアメロジェニンの歯周組織再生への複合的効果

    大和寛明、讃井彰一、四本かれん、中尾雄紀、渡邊ゆかり、林千華子、相原良亮、岩下未咲、田中麗、福田隆男、西村英紀

    2021年度日本歯科保存学会春季学術大会(第154回)  2021.6 

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    Event date: 2021.6

    Language:Japanese  

    Venue:Web開催   Country:Japan  

  • 歯肉幹細胞由来エクソソーム内包miR-1260bによる小胞体ストレス応答制御を介した抗炎症作用.

    林千華子、福田隆男、渡邊ゆかり、川上賢太郎、豊田真顕、中尾雄紀、四本かれん、大和寛明、新城尊徳、讃井彰一、西村英紀.

    第64回春季日本歯周病学会学術大会  2021.5 

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    Event date: 2021.5 - 2021.6

    Language:Japanese  

    Venue:Web開催   Country:Japan  

  • 歯肉幹細胞GMSC由来エクソソームによるCD73を介した免疫制御機構

    渡邊ゆかり、福田隆男、中尾雄紀、林千華子、川上賢太郎、豊田真顕、四本かれん、大和寛明、讃井彰一、西村英紀

    第153回日本歯科保存学会2020年度秋季学術大会  2020.11 

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    Event date: 2020.11

    Language:Japanese  

    Venue:Web開催   Country:Japan  

  • 歯肉幹細胞由来エクソソームは、miR-1260bによるRANKL阻害により歯槽骨吸収を抑制する

    中尾雄紀、福田隆男、渡邊ゆかり、林千華子、川上賢太郎、豊田真顕、四本かれん、大和寛明、新城尊徳、田中麗、讃井彰一、西村英紀

    第153回日本歯科保存学会2020年度秋季学術大会  2020.11 

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    Event date: 2020.11

    Language:Japanese  

    Venue:Web開催   Country:Japan  

  • Amelogenin down-regulates MHC class II antigen presentation on macrophages. International conference

    Karen Yotsumoto, Terukazu Sanui, Hiroaki Yamato, Urara Tanaka, Yuki Nakao, Chikako Hayashi, Hiroaki Yamato, Yukari Watanabe, Takao Fukuda, Fusanori Nishimura

    JADR, The 68th annual meeting  2020.11 

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    Event date: 2020.11

    Language:English  

    Venue:WEB開催   Country:Japan  

  • Exosomes from TNF-α-treated human gingiva-derived MSCs inhibit periodontal bone loss via miR-1260b-mediated RANKL inhibition. International conference

    Yuki Nakao, Takao Fukuda, Yukari Watanabe, Chikako Hayashi, Kentaro Kawakami, Masaaki Toyoda, Karen Yotsumoto, Hiroaki Yamato, Takanori Shinjyo, Urara Tanaka, Terukazu Sanui, Fusanori Nishimura.

    JADR, The 68th annual meeting  2020.11 

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    Event date: 2020.11

    Language:English  

    Venue:WEB開催   Country:Japan  

  • Amelogenin suppresses IFNγ-induced MHC class II expression in macrophages. International conference

    Karen Yotsumoto, Terukazu Sanui, Urara Tanaka, Hiroaki Yamato, Yuki Nakao, Yukari Watanabe, Chikako Hayashi, Takao Fukuda, Fusanori Nishimura

    American Academy of Periodontology (AAP), 106th Annual meeting  2020.11 

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    Event date: 2020.11

    Language:English  

    Venue:WEB開催   Country:United States  

  • Therapeutic potential of exosomes derived from GMSCs in periodontal disease. International conference

    Yuki Nakao, Takao Fukuda, Yukari Watanabe, Chikako Hayashi, Kentaro Kawakami, Masaaki Toyoda, Karen Yotsumoto, Hiroaki Yamato, Takanori Shinjyo, Urara Tanaka, Terukazu Sanui, Fusanori Nishimura.

    American Academy of Periodontology (AAP), 106th Annual meeting  2020.11 

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    Event date: 2020.11

    Language:English  

    Venue:WEB開催   Country:United States  

  • Combined application of geranylgeranylacetone and amelogenin promotes angiogenesis and wound healing in human periodontal ligament cells. International conference

    Hiroaki Yamato, Terukazu Sanui, Karen Yotsumoto, Yuki Nakao, Yukari Watanabe, Chikako Hayashi, Takao Fukuda, Urara Tanaka, Fusanori Nishimura.

    American Academy of Periodontology (AAP), 106th Annual meeting  2020.11 

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    Event date: 2020.11

    Language:English  

    Venue:WEB開催   Country:United States  

  • アメロジェニンはマクロファージにおけるCIITAのプロモーターIV領域のユークロマチン化を阻害しIFNγ誘導性誘導性のMHCクラスII抗原提示を抑制する.

    四本かれん、田中麗、讃井彰一、大和寛明、中尾雄紀、渡邊ゆかり、林千華子、福田隆男、西村英紀

    第63回秋季日本歯周病学会春季学術大会  2020.10 

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    Event date: 2020.10

    Language:Japanese  

    Venue:Web開催   Country:Japan  

  • Amelogenin inhibits IFNγ-induced MHC class II expression in macrophages. International conference

    Karen Yotsumoto, Urara Tanaka, Terukazu Sanui, Takao Fukuda, Chikako Hayashi, Yuki Nakao, Hiroaki Yamato, Yukari Watanabe, Fusanori Nishimura

    IADR General Session & Exhibition  2020.3 

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    Event date: 2020.3

    Language:English  

    Venue:Washington D.C., USA(誌上開催)   Country:United States  

  • Therapeutic potential of exosomes derived from GMSCs in periodontal disease. International conference

    Yuki Nakao, Takao Fukuda, Yukari Watanabe, Chikako Hayashi, Kentaro Kawakami, Masaaki Toyoda, Karen Yotsumoto, Hiroaki Yamato, Takanori Shinjo, Urara Tanaka, Terukazu Sanui, Fusanori Nishimura.

    IADR General Session & Exhibition  2020.3 

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    Event date: 2020.3

    Language:English  

    Venue:Washington D.C., USA(誌上開催)   Country:United States  

  • 胃潰瘍治療薬テプレノンとアメロジェニンによる歯周組織再生誘導の可能性

    大和寛明,讃井彰一,四本かれん,中尾雄紀,渡邊ゆかり,福田隆男,田中麗,西村英紀

    令和元年度日本歯周病学会九州五大学・日本臨床歯周病学会九州支部・合同研修会  2019.11 

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    Event date: 2019.11

    Language:Japanese  

    Venue:アクロス福岡、福岡市   Country:Japan  

  • アメロジェニンはマクロファージによるIFNγ誘導性MHCクラスⅡの抗原提示を抑制する

    四本かれん、田中麗、讃井彰一、大和寛明、中尾雄紀、渡邊ゆかり、林千華子、福田隆男、西村英紀

    令和元年度日本歯周病学会九州五大学・日本臨床歯周病学会九州支部・合同研修会  2019.11 

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    Event date: 2019.11

    Language:Japanese  

    Venue:アクロス福岡、福岡市   Country:Japan  

  • 歯肉幹細胞由来エクソソーム由来miR-1260bはWnt5aを介して歯根膜細胞におけるRANKL発現を抑制する。

    中尾雄紀、福田隆男、渡邊ゆかり、林千華子、四本かれん、大和寛明、田中麗、讃井彰一、西村英紀

    第151回秋季日本歯科保存学会秋季学術大会  2019.11 

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    Event date: 2019.11

    Language:Japanese  

    Venue:福岡国際会議場、福岡市   Country:Japan  

  • アメロジェニンはマクロファージにおけるIFNγ誘導性MHCクラスⅡ分子の発現を抑制する。

    四本かれん、田中麗、讃井彰一、大和寛明、中尾雄紀、渡邊ゆかり、林千華子、福田隆男、西村英紀

    第62回秋季日本歯周病学会学術大会  2019.10 

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    Event date: 2019.10 - 2019.6

    Language:Japanese  

    Venue:西日本総合展示場・北九州国際会議場、北九州市   Country:Japan  

  • アメロジェニンはマクロファージによる抗原提示を抑制させる。

    四本かれん、田中麗、讃井彰一、大和寛明、中尾雄紀、渡邊ゆかり、福田隆男、西村英紀

    第150回日本歯科保存学会春季学術大会  2019.6 

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    Event date: 2019.6

    Language:Japanese  

    Venue:石川県立音楽堂、金沢市   Country:Japan  

  • アメロジェニンおよび胃潰瘍治療薬テプレノンが歯根膜細胞機能に与える影響

    大和寛明、讃井彰一、四本かれん、中尾雄紀、渡邊ゆかり、福田隆男、田中麗、西村英紀

    第150回日本歯科保存学会春季学術大会  2019.6 

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    Event date: 2019.6

    Language:Japanese  

    Venue:石川県立音楽堂、金沢市   Country:Japan  

  • 歯肉幹細胞由来エクソソームは歯根膜細胞の RANKL 発現を抑制する。

    中尾雄紀、福田隆男、渡邊ゆかり、林千華子、四本かれん、大和寛明、田中麗、讃井彰一、西村英紀

    第62回春季日本歯周病学会学術大会  2019.5 

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    Event date: 2019.5

    Language:Japanese  

    Venue:神奈川県民ホール、横浜市   Country:Japan  

  • SPOCK-1 upregulation is a novel epithelial mesenchymal transition (EMT) inducer in calcium channel blocker-induced gingival overgrowth.

    Rehab Alshargabi, Tomomi Sano, Akiko Yamashita, Taiki Sanada, Takao Fukuda, Misaki Iwashita, Terukazu Sanui, Fusanori Nishimura

    第62回春季日本歯周病学会学術大会  2019.5 

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    Event date: 2019.5

    Language:English  

    Venue:神奈川県民ホール、横浜市   Country:Japan  

  • SPOCK-1 is a novel epithelial mesenchymal transition (EMT) inducer in calcium channel blocker-induced gingival overgrowth. International conference

    Rehab Alshargabi, Tomomi Sano, Akiko Yamashita, Taiki Sanada, Takao Fukuda, Misaki Iwashita, Terukazu Sanui, Fusanori Nishimura

    Kyudai Oral Bioscience & OBT Research Center Joint International Symposium  2019.3 

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    Event date: 2019.3

    Language:English  

    Venue:Fukuoka   Country:Japan  

  • SPOCK-1 is a novel epithelial mesenchymal transition (EMT) inducer in drug induced gingival overgrowth. International conference

    Rehab Alshargabi, Tomomi Sano, Akiko Yamashita, Taiki Sanada, Takao Fukuda, Misaki Iwashita, Terukazu Sanui, Fusanori Nishimura

    Korean Academy of Periodontology (KAP)  2019.3 

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    Event date: 2019.3

    Language:English  

    Venue:Seoul, South Korea   Country:Korea, Republic of  

  • 歯肉幹細胞由来エクソソームによる抗炎症性マクロファージ誘導機序の検討 ~間葉系幹細胞培養上清の有する抗炎症作用に注目して~

    中尾雄紀,福田隆男,讃井彰一,田中麗,渡邊ゆかり,大和寛明,四本かれん,西村英紀

    平成30年度日本歯周病学会九州五大学・日本臨床歯周病学会九州支部・合同研修会  2018.11 

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    Event date: 2018.11

    Language:Japanese  

    Venue:アクロス福岡、福岡市   Country:Japan  

  • The Role of Proteoglycans in Drug Induced Gingival Overgrowth (DIGO)

    Rehab Alshargabi, Tomomi Sano, Akiko Yamashita, Taiki Sanada, Takao Fukuda, Misaki Iwashita, Terukazu Sanui, Fusanori Nishimura

    第149回日本歯科保存学会2018年度秋季学術大会  2018.11 

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    Event date: 2018.11

    Language:English  

    Venue:みやこめっせ、京都市   Country:Japan  

  • 歯肉幹細胞由来エクソソームによる抗炎症性マクロファージ誘導機序の検討

    中尾雄紀,福田隆男,讃井彰一,田中麗,渡邊ゆかり,大和寛明,四本かれん,西村英紀

    第61回秋季日本歯周病学会学術大会  2018.7 

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    Event date: 2018.7

    Language:Japanese  

    Venue:リーガロイヤルホテル大阪、大阪市   Country:Japan  

  • Effect of amelogenin on antigen presentation in macrophages. International conference

    Urara Tanaka, Karen Yotsumoto, Terukazu Sanui, Takao Fukuda, Hiroaki Yamato, Yuki Nakao, Fusanori Nishimura

    96th General Session & Exhibition of the IADR  2018.7 

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    Event date: 2018.7

    Language:English  

    Venue:London   Country:United Kingdom  

  • 炎症脂肪/歯周組織における抗炎症分子の探索研究

    眞田大樹、佐野朋美、福田隆男、岩下未咲、山下明子、藤田剛、讃井彰一、栗原英見、西村英紀

    第148回日本歯科保存学会2018年度春季学術大会  2018.6 

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    Event date: 2018.6

    Language:Japanese  

    Venue:横浜みなとみらいホール、横浜市   Country:Japan  

  • The role of proteoglycans in the pathogenesis of drug induced gingival overgrowth (DIGO).

    Rehab Alshargabi, Aiko Takano, Akiko Yamashita, Misaki Iwashita, Takao Fukuda, Terukazu Sanui, Fusanori Nishimura

    第61回春季日本歯周病学会学術大会  2018.6 

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    Event date: 2018.6

    Language:Japanese  

    Venue:京王プラザホテル、東京都   Country:Japan  

  • アンジオポエチン様タンパク質2は骨芽細胞分化のpositive regulatorとして機能する。

    高野愛子、福田隆男、新城尊徳、岩下未咲、竹下正章、Rehab Alshargabi、讃井彰一、西村英紀

    日本歯周病学会60周年記念京都大会  2017.12 

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    Event date: 2017.12

    Language:Japanese  

    Venue:国立京都国際会館、京都市   Country:Japan  

  • The role of SPOCK-1 in Drug induced gingival overgrowth (DIGO)

    Rehab Alshargabi、高野愛子、山下明子、豊田敬介、岩下未咲、佐野朋美、鶴田満大、松永紘明、眞田大樹、竹下正章、相田 宜利、讃井彰一、西村英紀

    日本歯周病学会60周年記念京都大会  2017.12 

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    Event date: 2017.12

    Language:English  

    Venue:国立京都国際会館、京都市   Country:Japan  

  • Microarray analysis of U937 monocytic cells stimulated with amelogenin. International conference

    Urara Tanaka, Karen Yotsumoto, Terukazu Sanui, Takao Fukuda, Kyosuke Toyoda, Fusanori Nishimura

    Penn Periodontal Conference 2017  2017.6 

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    Event date: 2017.6

    Language:English  

    Venue:University of Pennsylvania, Philadelphia, PA, USA   Country:Japan  

  • 歯周炎モデルマウスにおける歯槽骨吸収及び破骨細胞分化へのDecitabineの効果

    田中麗、讃井彰一、福田隆男、西村英紀

    第146回日本歯科保存学会2017年度春季学術大会  2017.6 

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    Event date: 2017.6

    Language:Japanese  

    Venue:リンクステーションホール青森 青森市   Country:Japan  

  • アメロジェニンが有する抗炎症効果の機序解明

    山道研介、福田隆男、讃井彰一、豊田敬介、田中麗、西村英紀

    平成28年度日本歯周病学会九州五大学・日本臨床歯周病学会九州支部・合同研修会  2016.10 

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    Event date: 2016.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:長崎県歯科医師会館、長崎市   Country:Japan  

  • 骨組織におけるアンジオポエチン様タンパク質2の役割の機能解析

    高野愛子、福田隆男、新城尊徳、岩下未咲、讃井彰一、山道研介、竹下正章、西村英紀

    第145回日本歯科保存学会2016年度秋季学術大会  2016.10 

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    Event date: 2016.10

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:キッセイ文化ホール、松本市   Country:Japan  

  • IL-17Aは3T3-L1脂肪細胞におけるTNF-α誘導性IL-6・CCL20産生を相乗的に増強する。

    佐野朋美、新城尊徳、岩下未咲、山下明子、讃井彰一、西村英紀

    第145回日本歯科保存学会2016年度秋季学術大会  2016.10 

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    Event date: 2016.10

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:キッセイ文化ホール、松本市   Country:Japan  

  • Decitabineによる歯周炎モデルマウスにおける歯槽骨吸収抑制効果の検討

    田中麗、讃井彰一、福田隆男、西村英紀

    第59回秋季日本歯周病学会学術大会  2016.10 

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    Event date: 2016.10

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:朱鷺メッセ 新潟コンベンションセンター、新潟市   Country:Japan  

  • Spry2 knockdown enhances proliferation and migration but reduces differentiation of periodontal ligament cells through bFGF and EGF stimulation. International conference

    Hajime Akiyama, Urara Tanaka, Terukazu Sanui, Takao Fukuda, Kyosuke Toyoda, Kensuke Yamamichi, Takaharu Taketomi, Fusanori Nishimura.

    94th General Session & Exhibition of the International Association for Dental Research  2016.6 

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    Event date: 2016.6 - 2018.6

    Language:English  

    Venue:Seoul, South Korea   Country:Japan  

  • Grp78 is crucial for cell migration induced by amelogenin in a human periodontal ligament cells. International conference

    Kyosuke Toyoda, Hajime Akiyama, Takao Fukuda, Terukazu Sanui, Urara Tanaka, Takaharu Taketomi, Fusanori Nishimura

    94th General Session & Exhibition of the International Association for Dental Research  2016.6 

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    Event date: 2016.6 - 2018.6

    Language:English  

    Venue:Seoul, South Korea   Country:Japan  

  • Amelogenin Modulates Macrophage Phenotype During Inflammatory Responses. International conference

    Kensuke Yamamichi, Hajime Akiyama, Takao Fukuda, Terukazu Sanui, Kyosuke Toyoda, Urara Tanaka, Takaharu Taketomi, Fusanori Nishimura

    94th General Session & Exhibition of the International Association for Dental Research  2016.6 

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    Event date: 2016.6 - 2018.6

    Language:English  

    Venue:Seoul, South Korea   Country:Japan  

  • 骨組織におけるアンジオポエチン様タンパク質2の役割の解明

    高野愛子、福田隆男、新城尊徳、岩下未咲、讃井彰一、山道研介、竹下正章、西村英紀

    第144回日本歯科保存学会2016年度春季学術大会  2016.6 

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    Event date: 2016.6

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:栃木県総合文化センター   Country:Japan  

  • 歯周病感染器官培養モデルを用いた抗菌薬の効果に関する研究

    竹下正章、原口晃、三浦真由美、濱地貴文、福田隆男、讃井彰一、西村英紀

    第59回春季日本歯周病学会学術大会  2016.5 

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    Event date: 2016.5

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:かごしま県民交流センター、鹿児島市   Country:Japan  

  • Molecular basis of amelogenin-induced periodontal tissue regeneration. Invited International conference

    Takao Fukuda, Terukazu Sanui, Kyosuke Toyoda, Urara Tanaka, Kensuke Yamamichi, Ryo Atomura, Hajime Akiyama, Fusanori Nishimura

    「口腔から健康長寿を支えるプロジェクト推進に向けた研究拠点構築プログラム」2nd Symposium  2016.2 

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    Event date: 2016.2 - 2018.2

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:福岡リーセントホテル   Country:Japan  

  • Molecular basis of amelogenin-induced periodontal tissue regeneration International conference

    福田隆男, 讃井 彰一, 豊田敬介, 田中麗, 後村亮, 山道研介, 西村 英紀

    口腔から健康長寿を支えるプロジェクト推進に向けた研究拠点構築プログラム2nd Symposium  2016.2 

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    Event date: 2016.2

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Penn Dental Medicine in Philadelphia, Pennsylvania   Country:United States  

  • ヒト歯根膜幹細胞/前駆細胞株の細胞遊走時に及ぼす分子機構

    豊田敬介, 福田隆男, 讃井 彰一, 山道研介, 後村亮, 西村 英紀

    2015年度秋季学術大会 (143回) 第17回日韓歯科保存学会学術大会  2015.11 

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    Event date: 2015.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:文京シビックホール、東京都   Country:Japan  

  • アメロジェニンが炎症過程におけるマクロファージの形質転換におよぼす影響

    山道研介, 福田隆男, 讃井 彰一, 豊田敬介, 後村亮, 西村 英紀

    2015年度秋季学術大会 (143回) 第17回日韓歯科保存学会学術大会  2015.11 

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    Event date: 2015.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:文京シビックホール、東京都   Country:Japan  

  • Spry2抑制によるM1マクロファージへの分化抑制メカニズムの解析

    後村亮, 讃井 彰一, 福田隆男, 豊田敬介, 山道研介, 西村 英紀

    2015年度秋季学術大会 (143回) 第17回日韓歯科保存学会学術大会  2015.11 

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    Event date: 2015.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:文京シビックホール、東京都   Country:Japan  

  • アメロジェニンが有する抗炎症効果の機序解明

    山道研介, 福田隆男, 讃井 彰一, 豊田敬介, 後村亮, 西村 英紀

    平成27年度日本臨床歯周病学会九州支部・日本歯周病学会九州五大学合同研修会  2015.11 

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    Event date: 2015.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:アクロス福岡、福岡市   Country:Japan  

  • Grp78 Is Critical For Amelogenin-induced Cell Migration In PDLSCs International conference

    Takao Fukuda, 豊田敬介, 讃井 彰一, 田中麗, 山道研介, 後村亮, 西村 英紀

    The 63rd Annual Meeting of Japanese Association for Dental Research  2015.10 

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    Event date: 2015.10

    Language:English   Presentation type:Oral presentation (general)  

    Venue:福岡国際会議場   Country:Japan  

  • Inhibition of Sprouty2 Regulates Cell Functions in Periodontal Ligament Cells International conference

    田中麗, 讃井 彰一, 福田隆男, 豊田敬介, 後村亮, 山道研介, 西村 英紀

    Penn Periodontal Conference 2015  2015.6 

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    Event date: 2015.6 - 2015.7

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Penn Dental Medicine in Philadelphia, Pennsylvania   Country:United States  

  • Grp78 is critical for amelogenin-induced cell migration in PDL cells International conference

    福田隆男, 豊田敬介, 讃井 彰一, 後村亮, 山道研介, 田中麗, 西村 英紀

    Penn Periodontal Conference 2015  2015.6 

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    Event date: 2015.6 - 2015.7

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Penn Dental Medicine in Philadelphia, Pennsylvania   Country:United States  

  • Spry2がPorphyromonas gingivalis LPS刺激マクロファージの分化に及ぼす影響について

    後村亮, 讃井 彰一, 福田隆男, 豊田敬介, 山道研介, 田中麗, 西村 英紀

    日本歯科保存学会 2015年度春季学術大会  2015.6 

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    Event date: 2015.6

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:北九州国際会議場、北九州市   Country:Japan  

  • Spry2がPorphyromonas gingivalis LPS刺激マクロファージの分化に及ぼす影響について

    後村亮, 讃井 彰一, 福田隆男, 豊田敬介, 山道研介, 田中麗, 西村 英紀

    日本歯科保存学会 2015年度春季学術大会  2015.6 

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    Event date: 2015.6

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:北九州国際会議場、北九州市   Country:Japan  

  • 歯周病感染器官培養モデルを用いた抗菌薬の効果に関する研究

    竹下正章, 讃井 彰一, 西村 英紀

    第142回日本歯科保存学会 2015年度春季学術大会  2015.6 

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    Event date: 2015.6

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:北九州国際会議、北九州市   Country:Japan  

  • マクロファージにおけるアメロジェニン刺激の影響の網羅的遺伝子解析

    山道研介, 福田隆男, 讃井 彰一, 後村亮, 豊田敬介, 田中麗, 西村 英紀

    日本歯科保存学会 2015年度春季学術大会  2015.6 

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    Event date: 2015.6

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:北九州国際会議場、北九州市   Country:Japan  

  • 新規に同定したアメロジェニン会合蛋白Grp78がヒト歯根膜幹細胞/前駆細胞株の機能に及ぼす役割の検討

    豊田敬介, 後村亮, 福田隆男, 讃井 彰一, 山道研介, 田中麗, 西村 英紀

    平成27年度 第58回春季日本歯周病学会学術大会  2015.5 

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    Event date: 2015.5

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:幕張メッセ 国際会議場、千葉市   Country:Japan  

  • Grp78 is Essential for Amelogenin-Induced Cell Migration in PDLSCs. International conference

    福田隆男, 後村亮, 豊田敬介, 山道研介, 田中麗, 讃井 彰一, 西村 英紀

    93rd General Session & Exhibition of the International Association for Dental Research  2015.3 

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    Event date: 2015.3

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Haynes Convention Center, Boston   Country:United States  

  • Grp78 is critical for amelogenin-induced cell migration in a human periodontal ligament stem/progenitor cell line.

    豊田敬介, 讃井 彰一, 福田隆男, 田中麗, 後村亮, 山道研介, 西村 英紀

    Kyudai Oral Bioscience (KOB) 2015  2015.2 

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    Event date: 2015.2

    Language:English   Presentation type:Oral presentation (general)  

    Venue:福岡リーセントホテル、福岡市   Country:Japan  

  • Sprouty2 Regulates Cell Proliferation and Migration in Periodontal Ligament Cells.

    田中麗, 讃井 彰一, 福田隆男, 豊田敬介, 後村亮, 山道研介, 西村 英紀

    頭脳循環Kick Off Symposium  2015.2 

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    Event date: 2015.2

    Language:English   Presentation type:Oral presentation (general)  

    Venue:福岡リーセントホテル、福岡市   Country:Japan  

  • Kyosuke Toyoda, Takao Fukuda, Ryo Atomura, Terukazu Sanui, Urara Tanaka, Takaharu Taketomi, Kensuke Yamamichi and Fusanori Nishimura Amelogenin induces cell migration via Grp78 in PDL cells.

    豊田敬介, 後村亮, 福田隆男, 讃井 彰一, 山道研介, 田中麗, 西村 英紀

    62nd Annual Meeting of Japanese Association for Dental Research  2014.12 

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    Event date: 2014.12

    Language:English   Presentation type:Oral presentation (general)  

    Venue:KKRホテル大阪、大阪市   Country:Japan  

  • 歯周病感染器官培養モデルを用いた抗菌療法確立を目指す基礎研究

    竹下正章, 讃井 彰一, 西村 英紀

    平成 26 年度日本歯周病学会五大学・日本臨床歯周病学会九州支部合同研修会  2014.11 

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    Event date: 2014.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:アクロス福岡、福岡市   Country:Japan  

  • アメロジェニンの生物学的活性の機序解明

    豊田敬介, 後村亮, 福田隆男, 讃井 彰一, 山道研介, 田中麗, 西村 英紀

    平成26年度 日本歯周病学会九州五大学日本臨床歯周病学会九州支部合同研修会  2014.11 

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    Event date: 2014.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:アクロス福岡、福岡市   Country:Japan  

  • 歯周病感染器官培養モデルを用いた抗菌療法確立を目指す基礎研究

    竹下正章, 讃井 彰一, 西村 英紀

    第 104 回日本歯科保存学会秋季学術大会  2014.10 

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    Event date: 2014.10

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:山形テルサ、山形市   Country:Japan  

  • Aggregatibacter actinomycetemcomitans は菌体外にDNA-LPS 複合体を産生し、その病原性はLPS単体よりも低い

    竹下正章, 讃井 彰一, 西村 英紀

    第58日本歯周病学会秋季学術大会  2014.10 

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    Event date: 2014.10

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:神戸市国際展示場、神戸市   Country:Japan  

  • 新規に同定したアメロジェニン会合分子GRP78がヒト歯根膜細胞機能に果たす役割の検討

    豊田敬介, 後村亮, 福田隆男, 讃井 彰一, 山道研介, 田中麗, 西村 英紀

    第58日本歯周病学会秋季学術大会  2014.10 

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    Event date: 2014.10

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:神戸市国際展示場、神戸市   Country:Japan  

  • マクロファージにおけるアメロジェニン刺激が関与するpathwayの検討

    後村亮, 豊田敬介, 福田隆男, 讃井 彰一, 西村 英紀

    140回 日本歯科保存学会2014年度春季学術大会  2014.6 

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    Event date: 2014.6

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:滋賀県立劇場びわ湖ホール、大津市   Country:Japan  

  • 新規アメロジェニン会合分子GRP78がヒト歯根膜細胞に及ぼす影響

    豊田敬介, 田中麗, 福田隆男, 讃井 彰一, 後村亮, 山道研介, 西村 英紀

    140回 日本歯科保存学会2014年度春季学術大会  2014.6 

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    Event date: 2014.6

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:滋賀県立劇場びわ湖ホール、大津市   Country:Japan  

  • Spry2を標的とした歯周組織再生療法確立を目指す基礎研究

    田中麗, 豊田敬介, 讃井 彰一, 福田隆男, 後村亮, 山道研介, 西村 英紀

    第57日本歯周病学会春季学術大会  2014.5 

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    Event date: 2014.5

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:長良川国際会議場、岐阜市   Country:Japan  

  • プロテオーム解析によるアメロジェニン会合分子の検討

    福田隆男, 豊田敬介, 田中麗, 讃井 彰一, 後村亮, 山道研介, 西村 英紀

    第139回 日本歯科保存学会 秋季学術大会  2013.11 

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    Event date: 2013.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:秋田市   Country:Japan  

  • 新規アメロジェニン会合分子Grp78がヒト歯根膜細胞に及ぼす影響

    豊田敬介, 田中麗, 福田隆男, 讃井 彰一, 後村亮, 山道研介, 西村 英紀

    平成25年度日本歯周病学会九州五大学・日本臨床歯周病学会九州支部合同研修会  2013.11 

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    Event date: 2013.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:北九州市九州歯科大学   Country:Japan  

  • フレアーアウトを伴う歯周炎患者に歯周矯正を行った一症例

    福田隆男, 豊田敬介, 田中麗, 讃井 彰一, 後村亮, 山道研介, 西村 英紀

    第56回 秋季日本歯周病学会学術大会  2013.9 

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    Event date: 2013.9

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:前橋市   Country:Japan  

  • Grp78 mediates endocytosis of amelogenin International conference

    福田隆男, 豊田敬介, 田中麗, 讃井 彰一, 後村亮, 山道研介, 西村 英紀

    10th Asian Pacific Society of Periodontology Meeting  2013.9 

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    Event date: 2013.9

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Nara   Country:Japan  

  • Sprouty2 controls cell proliferation and migration in periodontal ligament cells. International conference

    田中麗, 豊田敬介, 讃井 彰一, 福田隆男, 後村亮, 山道研介, 西村 英紀

    10th Asian Pacific Society of Periodontology Meeting  2013.9 

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    Event date: 2013.9

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Nara   Country:Japan  

  • Identification of novel ameogenin-binding proteins by proteomics analysis International conference

    豊田敬介, 田中麗, 福田隆男, 讃井 彰一, 後村亮, 山道研介, 西村 英紀

    10th Asian Pacific Society of Periodontology Meeting  2013.9 

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    Event date: 2013.9

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Nara   Country:Japan  

  • Proteomic approach to identify the receptor for amelogenin. International conference

    豊田敬介, 田中麗, 福田隆男, 讃井 彰一, 武富孝治, 後村亮, 西村 英紀

    2nd meeting of IADR-APR  2013.8 

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    Event date: 2013.8

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Plaza Athenee, Bangkok   Country:Thailand  

  • The effect of Grp78 on cellular uptake of amelogenin. International conference

    福田隆男, 豊田敬介, 田中麗, 讃井 彰一, 武富孝治, 後村亮, 西村 英紀

    2nd meeting of IADR-APR  2013.8 

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    Event date: 2013.8

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Plaza Athenee, Bangkok   Country:Thailand  

  • Spry2 regulates cell proliferation and migration in periodontal ligament cells. International conference

    田中麗, 豊田敬介, 讃井 彰一, 福田隆男, 武富孝治, 後村亮, 西村 英紀

    2nd meeting of IADR-APR  2013.8 

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    Event date: 2013.8

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Plaza Athenee, Bangkok   Country:Thailand  

  • アメロジェニン会合タンパクのプロテオーム解析

    豊田敬介, 田中麗, 福田隆男, 讃井 彰一, 後村亮, 濱地 貴文, 前田 勝正, 西村 英紀

    第56回春季日本歯周病学会学術大会  2013.5 

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    Event date: 2013.5 - 2013.6

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:タワーホール船堀   Country:Japan  

  • The effects of Sprouty2 in periodontal ligament cell International conference

    Tanaka Urara, Toyoda Kyosuke, Sanui Terukazu, Fukuda Takao, Takaharu Taketomi, Atomura Ryo, Hamachi Takafumi, Maeda Katsumasa

    91nd General Session & Exhibition of the IADR  2013.3 

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    Event date: 2013.3

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Washington States Convention Center   Country:United States  

  • Proteomic approach to understanding endocytosis of amelogenin International conference

    Fukuda Takao, Toyoda Kyosuke, Tanaka Urara, Sanui Terukazu, Takaharu Taketomi, Atomura Ryo, Hamachi Takafumi, Maeda Katsumasa

    91nd General Session & Exhibition of the IADR  2013.3 

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    Event date: 2013.3

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Washington States Convention Center   Country:United States  

  • The Role of Sprouty2 Protein in Osteoblasts and Periodontal Ligament Cells International conference

    Urara Tanaka, Kyosuke Toyoda, Terukazu Sanui, Takao Fukuda, Ryo Atomura, Takafumi Hamachi, and Katsumasa Maeda

    Kyudai Oral Bioscience 2013 —7th International Symposium —  2013.3 

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    Event date: 2013.3

    Presentation type:Oral presentation (general)  

    Venue:Fukuoka Recent Hotel   Country:Japan  

  • Proteomic Approach to Understanding Endocytosis of Amelogenin International conference

    Kyosuke Toyoda, Urara Tanaka, Takao Fukuda, Terukazu Sanui, Ryo Atomura, Takafumi Hamachi and Katsumasa Maeda

    Kyudai Oral Bioscience 2013 —7th International Symposium —  2013.3 

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    Event date: 2013.3

    Presentation type:Oral presentation (general)  

    Venue:Fukuoka Recent Hotel   Country:Japan  

  • アメロジェニン結合タンパクのプロテオーム解析 International conference

    田中 麗,讃井彰一,福田隆男,豊田敬介,後村 亮,濱地貴文,前田勝正

    第22 回日本歯科医学会総会  2012.11 

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    Event date: 2012.11

    Venue:大阪国際会議場   Country:Japan  

  • Y-box結合タンパク質の骨芽細胞における動態解析

    福田 隆男, 豊田 敬介, 讃井 彰一, 田中 麗, 後村 亮, 濱地 貴文, 前田 勝正

    第22 回日本歯科医学会総会  2012.11 

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    Event date: 2012.11

    Language:Japanese  

    Venue:大阪国際会議場   Country:Japan  

  • Sprouty2 could be new therapeutic targets for periodontal tissue regeneration. International conference

    Kyosuke Toyoda, Urara Tanaka, Terukazu Sanui, Takao Fukuda, Ryou Atomura, Takafumi Hamachi, Katsumasa Maeda

    98th Annual Meeting American Academy of Periodontology in collaboration with the Japanese Society of Periodontology  2012.9 

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    Event date: 2012.9 - 2012.10

    Country:United States  

  • Proteome analysis of amelogenin-binding proteins. International conference

    Urara Tanaka, Takao Fukuda, Terukazu Sanui, Kyosuke Toyoda, Takaharu Taketomi, Ryo Atomura, Takafumi Hamachi and Katsumasa Maeda

    Pan Europe Region ⁄ International Association for Dental Research (PER⁄IADR) Meeting  2012.9 

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    Event date: 2012.9 - 2012.11

    Venue:Finlandia Hall   Country:Finland  

  • Knockdown of YB-1 protein induces osteoblastic differentiation. International conference

    Takao Fukuda, Kyousuke Toyoda, Terukazu Sanui, Urara Tanaka, Takaharu Taketomi, Ryou Atomura, Takafumi Hamachi and Katsumasa Maeda

    Pan Europe Region ⁄ International Association for Dental Research (PER⁄IADR) Meeting  2012.9 

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    Event date: 2012.9 - 2012.11

    Venue:Finlandia Hall   Country:Finland  

  • Zoledronic acids enhance lipopolysaccharide-stimulated pro-inflammatory activation in macrophages. International conference

    D. MURATSU, D. YOSHIGA, T. TAKETOMI, T. ONIMURA, T. SANUI and S. NAKAMURA

    Pan Europe Region / International Association for Dental Research (PER/IADR)Meeting  2012.9 

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    Event date: 2012.9

    Venue:Finlandia Hall   Country:Finland  

  • Sprouty2 controls osteoblast proliferation and differentiation via FGF signaling. International conference

    T. ONIMURA, T. TAKETOMI, D. YOSHIGA, D. MURATSU, T. SANUI, T. FUKUDA, and S. NAKAMURA

    Pan Europe Region / International Association for Dental Research (PER/IADR)Meeting  2012.9 

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    Event date: 2012.9

    Venue:Finlandia Hall   Country:Finland  

  • Sprouty2を標的とした歯周組織再生の可能性

    田中麗、讃井彰一、福田隆男、豊田敬介、濱地貴文、前田勝正

    第55回春季日本歯周病学会学術大会  2012.5 

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    Event date: 2012.5

    Presentation type:Oral presentation (general)  

    Venue:札幌コンベンションセンター   Country:Japan  

  • Sprouty2分子を標的とした歯周組織再生の可能性

    田中麗、讃井彰一、福田隆男、豊田敬介、濱地貴文、前田勝正

    平成23年度日本歯周病学会九州五大学・日本臨床歯周病学会九州支部合同研修会  2011.11 

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    Event date: 2011.11

    Presentation type:Oral presentation (general)  

    Venue:長崎県歯科医師会館   Country:Japan  

  • ヒトY-box結合タンパク(YB-1)の骨芽細胞における細胞動態解析

    福田隆男、田中麗、讃井彰一、豊田敬介、久保田祥平、武富孝治、濱地貴文、前田勝正

    第54回日本歯周病学会秋季学術大会  2011.9 

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    Event date: 2011.9

    Presentation type:Oral presentation (general)  

    Venue:海峡メッセ下関   Country:Japan  

  • Sprouty2 controls the palate mesenchymal cell proliferation via FGF signaling. International conference

    K. MATSUMURA, T. TAKETOMI, K. YOSHIZAKI, S. ARAI, M. MORIYAMA, T. MAEHARA, T. SANUI, D. YOSHIGA, A. YOSHIMURA, and S. NAKAMURA.

    The 89th General Session and Exhibition of the IADR  2011.3 

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    Event date: 2011.3

    Presentation type:Oral presentation (general)  

    Venue:San Diego Convention Center   Country:United States  

  • Characterization of the amelogenin binding proteins. International conference

    Takao Fukuda, Terukazu Sanui, Takaharu Taketomi, Takafumi Hamachi and Katsumasa Maeda

    96th AAP annual meeting  2010.11 

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    Event date: 2010.10 - 2010.11

    Presentation type:Oral presentation (general)  

    Venue:Hawaii Convention Center   Country:United States  

  • YB-1 is important for amelogenin induced periodontal regeneration. International conference

    T. FUKUDA, T. SANUI, T. TAKETOMI, T. HAMACHI and K. MAEDA

    The 88th International Association for Dental Research (IADR)  2010.7 

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    Event date: 2010.7

    Presentation type:Oral presentation (general)  

    Venue:Center Conventions International Barcelona (CCIB)   Country:Spain  

  • Spry2 deficient mice exhibit cleft palate. International conference

    K. MATSUMURA, T. TAKETOMI, K. YOSHIGA, S. ARAI, T. SANUI and S. NAKAMURA

    The 88th International Association for Dental Research (IADR)  2010.7 

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    Event date: 2010.7

    Presentation type:Oral presentation (general)  

    Venue:Center Conventions International Barcelona (CCIB)   Country:Spain  

  • Sprouty2 accelerates the growth of ameloblastoma with EGF stimulation. International conference

    T. TAKETOMI, D. YOSHIGA, K. MITSUYASU, T. SANUI, T. FUKUDA, A. YOSHIMURA and S. NAKAMURA

    The 88th International Association for Dental Research (IADR)  2010.7 

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    Event date: 2010.7

    Presentation type:Oral presentation (general)  

    Venue:Center Conventions International Barcelona (CCIB)   Country:Spain  

  • Analysis of the molecular mechanisms of periodontal regeneration by EMD International conference

    Takao Fukuda, Terukazu Sanui, Takaharu Taketomi, Takafumi Hamachi, Katsumasa Maeda

    第5回 歯学研究院『口腔生命科学』国際シンポジウム  2010.2 

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    Event date: 2010.2

    Presentation type:Oral presentation (general)  

    Venue:九州大学医学部 百年講堂   Country:Japan  

  • Analysis of the novel protein bound to amelogenin in periodontal tissue cells. International conference

    Fukuda, T., Sanui, T., Taketomi, T., Hamachi, T., Maeda, K.

    The 50th Anniversary of Korean Academy of Conservative Dentistry, 2009 Autumn Scientific Meeting (the 132nd) and The 11th Joint-Scientific Meeting between KACD & JSCD  2009.11 

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    Event date: 2009.11

    Presentation type:Oral presentation (general)  

    Venue:Ramada Plaza, Jeju   Country:Korea, Republic of  

  • 歯周組織細胞群における新規アメロジェニン結合タンパク質の検索

    福田隆男、讃井彰一、武富孝治、後藤英文、濱地貴文、前田勝正

    日本歯周病学会  2009.5 

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    Event date: 2009.5

    Venue:岡山コンベンションセンター   Country:Japan  

    Analysis of the nobel protein bound to amelogenin in periodontal tissue cells.

  • DOCK2はNKT細胞の分化に必須である

    國崎祐也、讃井彰一、福井宣規

    日本免疫学会  2003.12 

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    Venue:第33回日本免疫学会総会・学術集会 福岡   Country:Japan  

  • 胸腺でのT細胞レパートリー形成が末梢の免疫応答に及ぼす質的影響

    大野隆真、福井宣規、讃井彰一、笹月健彦

    日本免疫学会  1999.12 

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    Venue:第29回日本免疫学会総会・学術集会 京都   Country:Japan  

  • 選択に関わる抗原ペプチドの構造によって影響されるT細胞レパートリーの多様性と特異性

    福井宣規、大野隆真、讃井彰一、笹月健彦

    日本免疫学会  1999.12 

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    Venue:第29回日本免疫学会総会・学術集会 京都   Country:Japan  

  • 造血系細胞特異的に発現するCDMファミリー遺伝子の単離とその機能解析

    福井宣規、大野隆真、讃井彰一、笹月健彦

    日本免疫学会  2000.11 

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    Venue:第30回日本免疫学会総会・学術集会 仙台   Country:Japan  

  • 自然発症末梢神経特異的自己免疫疾患マウスモデルの樹立とその発症におけるT細胞レパートリー選択の関与

    大野隆真、福井宣規、讃井彰一、笹月健彦

    日本免疫学会  2000.11 

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    Venue:第30回日本免疫学会総会・学術集会 仙台   Country:Japan  

  • 単一MHC/ペプチド複合体上で分化したT細胞が末梢で自己及びアロMHC分子の拘束下で認識する抗原ペプチドの同定

    大野隆真、福井宣規、讃井彰一、笹月健彦

    日本免疫学会  2001.12 

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    Venue:第31回日本免疫学会総会・学術集会 大阪   Country:Japan  

  • 生物学的歯髄鎮静法確立の試み 炎症惹起分子の同定から歯内-歯周病変モデルでの検証まで

    川上 賢太郎, 渡邊 ゆかり, 林 千華子, 豊田 真顕, 新城 尊徳, 讃井 彰一, 福田 隆男, 西村 英紀

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2022.10  (NPO)日本歯科保存学会

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  • 歯肉幹細胞由来エクソソーム内包miR-1260bによる小胞体ストレス応答制御を介した歯周炎骨吸収抑制効果

    林 千華子, 福田 隆男, 渡邊 ゆかり, 川上 賢太郎, 豊田 真顕, 中尾 雄紀, 四本 かれん, 大和 寛明, 新城 尊徳, 讃井 彰一, 西村 英紀

    日本歯周病学会会誌  2022.5  (NPO)日本歯周病学会

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  • 幹細胞を用いたscaffold freeの骨様組織3D構造体の作製(Fabrication of stem cell-based scaffold-free bone-like 3D structures)

    Toyoda Masaaki, Kajioka Shunichi, Fujimoto Ryota, Hayashi Chikako, Kawakami Kentarou, Watanabe Yukari, Nakao Yuki, Yotumoto Karen, Sanui Terukazu, Fukuda Takao, Nakayama Koichi, Nishimura Fusanori

    日本歯周病学会会誌  2022.12  (NPO)日本歯周病学会

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  • 内皮のインスリン抵抗性は糖尿病関連歯周炎の増悪に関与する(Endothelial insulin resistance contributes to the exacerbation of diabetes-related periodontitis)

    Zeze Tatsuro, Shinjo Takanori, Sato Kohei, Imagawa Mio, Nishimura Yuki, Iwashita Misaki, Fukuda Takao, Sanui Terukazu, Nishimura Fusanori

    日本歯周病学会会誌  2022.12  (NPO)日本歯周病学会

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  • ヒト歯髄細胞由来マイクロベジクル含有PKRを標的とした歯髄鎮静薬および歯内・歯周病変モデルの作成に向けて

    川上 賢太郎, 渡邊 ゆかり, 林 千華子, 豊田 真顕, 新城 尊徳, 讃井 彰一, 福田 隆男, 西村 英紀

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2022.5  (NPO)日本歯科保存学会

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  • バイオ3Dプリンターを用いた歯肉幹細胞由来骨様立体構造物の作製方法の確立と骨分化能,石灰化度に関する解析

    豊田 真顕, 梶岡 俊一, 福田 隆男, 川上 賢太郎, 信太 実有, 李 金鳳, 林 千華子, 中尾 雄紀, 讃井 彰一, 西村 英紀

    日本歯周病学会会誌  2023.10  (NPO)日本歯周病学会

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  • バイオ3Dプリンターを用いた、間葉系幹細胞からの骨様立体構造物作製への挑戦

    豊田 真顕, 梶岡 俊一, 福田 隆男, 渡邊 ゆかり, 林 千華子, 川上 賢太郎, 中尾 雄紀, 四本 かれん, 大和 寛明, 讃井 彰一, 西村 英紀

    日本歯周病学会会誌  2022.5  (NPO)日本歯周病学会

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  • エムドゲインのプロテオミクス

    福田 隆男, 川上 賢太郎, 王 紫瑜, 肖 萌, 豊田 真顕, 林 千華子, 信太 実有, 李 金鳳, Mwannes Ahmad, 讃井 彰一, 西村 英紀

    日本歯周病学会会誌  2024.4  (NPO)日本歯周病学会

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  • アメロジェニンが他家皮膚移植モデルマウスの拒絶反応に及ぼす影響

    信太 実有, 讃井 彰一, 西村 優輝, 林 千華子, 川上 賢太郎, 豊田 真顕, 新城 尊徳, 福田 隆男, 西村 英紀

    日本歯周病学会会誌  2024.4  (NPO)日本歯周病学会

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  • TNF-α/IFN-α共刺激した歯肉幹細胞由来エクソソームはCD73とCD5Lを介して抗炎症性M2マクロファージを誘導する

    渡邊 ゆかり, 林 千華子, 川上 賢太郎, 豊田 真顕, 中尾 雄紀, 大和 寛明, 四本 かれん, 新城 尊徳, 岩下 未咲, 讃井 彰一, 福田 隆男, 西村 英紀

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2022.5  (NPO)日本歯科保存学会

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  • Skp1を標的としNF-κBシグナルを介した炎症を抑制するmiR-582-5pは歯周炎と肥満において抑制されている(miR-582-5p, that targets Skpl and suppresses NF-κB signaling-mediated inflammation, is down-regulated in periodontitis and obesity)

    Li Rongzhi, Sano Tomomi, Fukuda Takao, Shinjo Takanori, Iwashita Misaki, Yamashita Akiko, Sanui Terukazu, Nishimura Fusanori

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2023.5  (NPO)日本歯科保存学会

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  • ATF6βを標的としたmiR-1260bの歯周病による量吸収抑制効果(miR-1260b inhibits periodontal bone loss by targeting ATF6β)

    Hayashi Chikako, Kawakami Kentaro, Toyoda Masaaki, Watanabe Yukari, Nakao Yuki, Yotsumoto Karen, Yamato Hiroaki, Shinjo Takanori, Sanui Terukazu, Fukuda Takao, Nishimura Fusanori

    日本歯周病学会会誌  2022.12  (NPO)日本歯周病学会

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MISC

  • 口腔内細菌および腸内細菌が増悪させる全身疾患の新知見

    讃井彰一

    福岡県歯科医師会「歯界時報」学術レポート   2022.9

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    Language:Japanese  

  • EMD Science Flash「Emdogain Gelの炎症抑制効果」

    讃井彰一, 四本かれん, 西村英紀.

    ストローマンジャパン   2020.9

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  • ミニレビュー 組織再生を目的としたアメロジェニン研究の現在

    讃井彰一、西村英紀

    日本歯周病学会誌   2019.9

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  • ザ・ペリオドントロジー第3版 第4章 歯周病の検査・診断と治療

    讃井彰一, 四本かれん, 西村英紀.

    永末書店   2019.2

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    Language:Japanese  

  • 細胞骨格制御分子を標的とした新規歯周治療法の開発に関する基礎的研究

    讃井彰一

    日本歯周病学会誌   2018.9

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    DOI: doi.org/10.2329/perio.60.117

  • Diabetes as a risk factor for periodontal disease-plausible mechanisms. Reviewed

    Polak D, Sanui T, Nishimura F, Shapira L.

    Periodontology 2000   2020.6

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    DOI: doi: 10.1111/prd.12298.

  • Glucose-regulated protein78: A therapeutic target for amelogenin-induced periodontal tissue regeneration.

    Fukuda T and Sanui T*, Toyoda K, Tanaka U, Yamamichi K, Taketomi T, Nishimura F.

    Single-Cell Biology   2016.6

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    DOI: doi:10.4172/2168-9431.1000137

  • New therapeutic strategy for regenerating periodontal tissue based on the combination of amelogenin and reapplications of existing Grp78 inducer.

    Fukuda T and Sanui T*, Toyoda K, Tanaka U, Yamamichi K, Taketomi T, Nishimura F.

    Journal of Cell Signaling   2016.6

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    DOI: doi:10.4172/jcs.1000118.

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Professional Memberships

  • Japanese Society for Immunology

  • International Association for Dental Research

  • Japan Asssociation of Dental Research

  • Japanese Society of Periodontology

  • Japanese Society of Conservative Dentistry

Committee Memberships

  • 日本歯周病学会   Steering committee member   Domestic

    2023.4 - 2025.3   

  • 日本歯周病学会   国際交流委員   Domestic

    2023.4 - 2025.3   

  • 日本歯周病学会   Steering committee member   Domestic

    2021.4 - 2023.3   

  • 日本歯周病学会   Steering committee member   Domestic

    2021.4 - 2023.3   

  • 日本歯周病学会   ペリオドンタルメディシン委員   Domestic

    2021.4 - 2023.3   

  • 日本歯周病学会   国際交流委員   Domestic

    2021.4 - 2023.3   

  • 日本歯周病学会   Steering committee member   Domestic

    2019.4 - 2021.3   

  • 日本歯周病学会   Steering committee member   Domestic

    2019.4 - 2021.3   

  • 日本歯周病学会   Steering committee member   Domestic

    2019.4 - 2021.3   

  • 日本歯周病学会   研究委員   Domestic

    2019.4 - 2021.3   

  • 日本歯周病学会   ペリオドンタルメディシン委員   Domestic

    2019.4 - 2021.3   

  • 日本歯周病学会   国際交流委員   Domestic

    2019.4 - 2021.3   

  • 日本歯周病学会   Steering committee member   Domestic

    2017.4 - 2019.3   

  • 日本歯周病学会   Steering committee member   Domestic

    2017.4 - 2019.3   

  • 日本歯周病学会   Steering committee member   Domestic

    2017.4 - 2019.3   

  • 日本歯周病学会   選挙管理委員   Domestic

    2017.4 - 2019.3   

  • 日本歯周病学会   研究委員   Domestic

    2017.4 - 2019.3   

  • 日本歯周病学会   国際交流委員   Domestic

    2017.4 - 2019.3   

  • 日本歯周病学会   Councilor   Domestic

    2016.4 - 2029.3   

  • 日本歯科保存学会   編集連絡委員   Domestic

    2015.4 - 2016.5   

  • 日本歯周病学会   編集連絡委員   Domestic

    2015.4 - 2016.5   

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Academic Activities

  • Screening of academic papers

    Role(s): Peer review

    2023

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:1

  • Screening of academic papers

    Role(s): Peer review

    2022

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:2

  • 準備委員長 International contribution

    The 69rd Annual Meeting of Japanese Association for Dental Research  ( Japan ) 2021.10

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    Type:Competition, symposium, etc. 

  • Screening of academic papers

    Role(s): Peer review

    2021

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:10

  • Screening of academic papers

    Role(s): Peer review

    2020

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:8

  • 準備委員長

    日本歯周病学会第1回佐賀地区臨床研修会  ( Japan ) 2019.2

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    Type:Competition, symposium, etc. 

    Number of participants:50

  • Screening of academic papers

    Role(s): Peer review

    2019

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:1

  • 座長

    日本歯周病学会 若手研究者の集い  ( Japan ) 2018.5

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    Type:Competition, symposium, etc. 

  • Screening of academic papers

    Role(s): Peer review

    2018

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:1

  • 準備委員長

    第60回日本歯周病学会春季学術大会  ( Japan ) 2017.5

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    Type:Competition, symposium, etc. 

    Number of participants:2,800

  • Screening of academic papers

    Role(s): Peer review

    2017

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:3

  • シンポジスト International contribution

    The 63rd Annual Meeting of Japanese Association for Dental Research  ( Japan ) 2015.10

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    Type:Competition, symposium, etc. 

  • 日本歯科保存学会会誌

    2015.4 - 2026.3

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    Type:Academic society, research group, etc. 

  • 日本歯周病学会会誌

    2015.4 - 2026.3

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    Type:Academic society, research group, etc. 

  • シンポジスト International contribution

    Kyudai Oral Bioscience 2013 —7th International Symposium —  ( Fukuoka Recent Hotel Japan ) 2013.3

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    Type:Competition, symposium, etc. 

  • メイン会場責任者

    第52回秋季日本歯周病学会学術大会  ( Japan ) 2009.10

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    Type:Competition, symposium, etc. 

▼display all

Research Projects

  • Spatial transcriptome analysis of GMSC-derived exoxme mediated peridontal tissue regneration

    Grant number:24K02623  2024.4 - 2028.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    福田 隆男, 西村 英紀, 讃井 彰一, 新城 尊徳, 武富 孝治

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    Grant type:Scientific research funding

    再生療法の代表的なツールである間葉系幹細胞(MSC)について、近年、細胞外分泌物であるエクソソームによる治療効果が近年示唆されている。本研究では申請者が独自に基礎研究を行ってきた歯肉幹細胞(GMSC)由来エクソソームを応用した革新的歯周組織再生療法の開発のため、①GMSC由来エクソソームによって特異的に誘導されるM2マクロファージの特徴および分化系譜の分子機序を見出し、②エクソソームを応用した組織再生プロセスの全容解明に向け空間トランスクリプトームデータを構築することで、M2マクロファージと近隣細胞間のネットワークの理解を図り、新規歯周組織再生療法に質する開発基盤を築くことを目的とする。

    CiNii Research

  • Challenge to periodontal tissue regeneration and refractory immune diseases based on amelogenin-CRP78 complex

    Grant number:23K27774  2024 - 2026

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    讃井 彰一, 福田 隆男, 武富 孝治, 西村 英紀

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    Authorship:Principal investigator  Grant type:Scientific research funding

    アメロジェニン・GRP78複合体がどのような機序で細胞内に移行し、免疫抑制および創傷治癒・血管新生を促進するのかは依然として不明である。
    本研究はアメロジェニン・GRP78複合体がこれらの機能を制御する分子基盤を解明するため、1.複合体の構造解析により複合体の細胞内移行の機序や生理的機能を解明することと、また2.GRP78発現を増強する化合物、テプレノンにより複合体の活性増強が可能か否かを検証することを目的としている。
    これらの結果をもって、テプレノンとアメロジェニンの複合投与による3.新しい歯周組織再生療法を開発すると共に、4.難治性免疫疾患の新規治療確立に向け研究のさらなる展開を図る。

    CiNii Research

  • 歯肉幹細胞由来エクソソームによる新規歯周病治療の開発

    2024 - 2025

    【シーズA310】令和6年度AMED橋渡し研究プログラム シーズA研究開発費

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    Authorship:Coinvestigator(s)  Grant type:On-campus funds, funds, etc.

  • アメロジェニン・CRP78複合体を基軸とした歯周組織再生と難治性免疫疾患への挑戦

    Grant number:23H03084  2023

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • 令和5年第12回小林財団研究助成

    2023

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    Grant type:Donation

  • NSKナカニシ財団2023年度研究開発助成

    2023

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    Grant type:Donation

  • Sprouty2 による上皮間葉転換制御を介した扁平上皮癌転移抑制機構の解明

    Grant number:20K10173  2020.4 - 2025.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    武富 孝治, 讃井 彰一, 福田 隆男

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    Grant type:Scientific research funding

    近年、癌の分子標的薬の発展は目覚ましく、細胞表層の受容体に対するモノクローナル抗体や MEK 阻害剤に代表されるような細胞内の分子をターゲットとした分子標的薬も次々と開発されている。本研究では、細胞のチロシンキナーゼ型受容体の下流で細胞内シグナル伝達を制御する Sprouty2 に着目し、口腔扁平上皮癌細胞の上皮間葉転換 (EMT) における Sprouty2 の作用を解析する。口腔扁平上皮癌のリンパ行性転移機構において Sprouty2 が E-cadherin などの細胞接着分子の発現変化や、浸潤性発育にどのような影響を与えるかを in vitro の実験で調べる。

    CiNii Research

  • New therapeutic strategy for periodontal disease targeting exosomal miRNA derived from GMSCs.

    Grant number:20H03865  2020.4 - 2024.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    福田 隆男, 武富 孝治, 新城 尊徳, 讃井 彰一, 西村 英紀

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    Grant type:Scientific research funding

    幹細胞による疾病治療効果には、幹細胞から分泌されるエクソソームと呼ばれる細胞分泌小胞が中心的役割を果たしており、エクソソームに内包されるmiRNAが損傷組織の遺伝子発現を制御することで治癒を促進することが明らかにされつつある。申請者らは歯肉幹細胞が分泌するエクソソームの有する著明な抗炎症・創傷治癒促進効果を発見したが、その詳細な分子基盤は不明である。
    本研究は、歯肉幹細胞由来エクソソームmiRNAを新たな核酸創薬ターゲットとした新規歯周治療の分子基盤を確立することで、最小限の幹細胞から歯周病の炎症の収束・組織リモデリング・再生シグナルを効果的に誘導する革新的歯周治療法の確立を目指す。

    CiNii Research

  • 歯肉幹細胞由来エクソソームmicroRNAを標的とした次世代歯周病治療の構築

    2020 - 2023

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

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    Authorship:Coinvestigator(s)  Grant type:Scientific research funding

  • The development of periodontal and endodontal tissue regenetation targeted amelogenin/GRP78 complex

    Grant number:20K09958  2020 - 2023

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    讃井 彰一, 福田 隆男, 武富 孝治

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    Authorship:Principal investigator  Grant type:Scientific research funding

    本研究はアメロジェニン・GRP78複合体が免疫応答や創傷治癒等に与える影響、およびそこに至るまでの分子メカニズムを解明するため、複合体の構造解析により複合体の核内移行の機序や生理的機能を解明することと、またGRP78を誘導するテプレノンにより、人為的にこの複合体の活性増強が可能かを検証することを目的としている。これらの結果をもって、テプレノンとアメロジェニンの複合投与による新しい歯周組織再生療法を開発すると共に、歯髄の再生に応用可能か否かについて研究の展開を図る。

    CiNii Research

  • Sprouty2 による上皮間葉転換制御を介した扁平上皮癌転移抑制機構の解明

    2020 - 2022

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Authorship:Coinvestigator(s)  Grant type:Scientific research funding

  • アメロジェニン・GRP78複合体を標的とした歯周歯髄組織再生技術の創生

    2017.4 - 2022.3

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    Authorship:Principal investigator 

  • 歯肉幹細胞由来エクソソームを用いた新規歯周病治療の開発

    2017 - 2019

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Authorship:Coinvestigator(s)  Grant type:Scientific research funding

  • チロシンキナーゼ阻害分子Sproutyによる口腔癌リンパ節転移制御機構の解明

    2017 - 2019

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Authorship:Coinvestigator(s)  Grant type:Scientific research funding

  • 炎症の収束と組織リモデリングを誘導する次世代歯周組織再生治療法の構築

    Grant number:17K11986  2017 - 2019

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • 財団法人武田科学振興財団 2017年度医学系研究奨励金

    2017

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    Grant type:Donation

  • 歯周医学の新展開~歯周炎症とエネルギー代謝の連関

    2016 - 2020

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

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    Authorship:Coinvestigator(s)  Grant type:Scientific research funding

  • M2マクロファージ転換技術を応用した新規歯周組織再生療法の開発

    Grant number:26463136  2014 - 2016

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • FGF抑制因子Sprouty /Spred によるエナメル上皮腫増殖制御機構の解明

    2014 - 2016

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Authorship:Coinvestigator(s)  Grant type:Scientific research funding

  • 新規アメロジェニン会合蛋白の分子基盤構築による歯周組織再生の創薬標的分子の同定

    2014 - 2016

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Authorship:Coinvestigator(s)  Grant type:Scientific research funding

  • 歯髄細胞由来TNF誘導因子(DPTIF)受容体の探索研究

    2014 - 2016

    Grants-in-Aid for Scientific Research  Grant-in-Aid for challenging Exploratory Research

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    Authorship:Coinvestigator(s)  Grant type:Scientific research funding

  • 平成26年度 学術研究振興基金助成金/FGF抑制因子Sprouty/Spred によるエナメル上皮腫増殖制御機構の解明

    2014

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    Grant type:Donation

  • bFGFシグナル伝達のアンタゴニストを標的とした歯周組織再生治療薬の創薬

    Grant number:24792334  2012 - 2013

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Young Scientists (B)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • PGRP-Sによる粘膜免疫制御機構の解明

    2011

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    Grant type:Donation

  • Sproutyを分子標的薬とした歯周組織再生療法の発明

    Grant number:22792092  2010 - 2011

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Young Scientists (B)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • 新規アメロジェニン会合分子を標的とした歯周組織再生療法の発明

    2009.4 - 2012.3

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    Authorship:Coinvestigator(s) 

  • 財団法人武田科学振興財団 2009年度医学系研究奨励金

    2009

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    Grant type:Donation

  • 塩基性線維芽細胞成長因子(bFGF)シグナルのアンタゴニストを標的とした歯周組織再生療法の開発

    2009

    平成21年度九州大学教育研究プログラム・研究拠点形成 プロジェクト

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    Authorship:Principal investigator  Grant type:On-campus funds, funds, etc.

  • 増殖シグナル制御分子Sproutyを標的とした歯周組織再生療法の開発

    2008.4 - 2012.3

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    Authorship:Principal investigator 

  • 増殖シグナル制御分子Sproutyを標的とした歯周組織再生療法の開発

    Grant number:20890161  2008 - 2009

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Young Scientists (Start-up)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • 歯周疾患における細胞骨格関連分子を標的とした免疫応答制御法の開発

    Grant number:17・5886  2005 - 2007

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for JSPS Fellows

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • チロシンキナーゼ阻害分子 Sprouty による口腔癌リンパ節転移制御機構の解明

    Grant number:17K11692 

    武富 孝治, 讃井 彰一, 福田 隆男

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    Grant type:Scientific research funding

    Sproutyファミリーは EGF や TGF-βによる刺激よりも FGF により発現誘導されるが、その機能はチロシンキナーゼ型受容体下流のシグナル伝達機構の制御のみならず、上皮間葉転換と深く関わりのある TGF-βシグナル伝達機構における Smad1/5/8 のリン酸化も抑制することが示され、上皮間葉転換を負に制御する可能性を見いだすことができた。また、Raft においてMAPキナーゼ経路のみで作用する Caveolin との結合は、Spry ドメインのシステイン rich な領域が関与しており、TGF-βシグナルの抑制は Caveolin 非依存的に作用することが示唆された。

    CiNii Research

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Class subject

  • 歯周病学Ⅰ

    2023.10 - 2024.3   Second semester

  • 臨床実習

    2023.4 - 2024.3   Full year

  • 臨床予備実習

    2023.4 - 2023.9   First semester

  • 歯周病学Ⅱ

    2023.4 - 2023.9   First semester

  • 歯周病学Ⅰ

    2022.10 - 2023.3   Second semester

  • 臨床実習

    2022.4 - 2023.3   Full year

  • 臨床予備実習

    2022.4 - 2022.9   First semester

  • 歯周病学Ⅱ

    2022.4 - 2022.9   First semester

  • 歯周病学Ⅰ

    2021.10 - 2022.3   Second semester

  • 臨床実習

    2021.4 - 2022.3   Full year

  • 臨床予備実習

    2021.4 - 2021.9   First semester

  • 歯周病学Ⅱ

    2021.4 - 2021.9   First semester

  • 歯周病学Ⅰ

    2020.10 - 2021.3   Second semester

  • 臨床実習

    2020.4 - 2021.3   Full year

  • 臨床予備実習

    2020.4 - 2020.9   First semester

  • 歯周病学Ⅱ

    2020.4 - 2020.9   First semester

  • 歯周病学Ⅰ

    2019.10 - 2020.3   Second semester

  • 臨床実習

    2019.4 - 2020.3   Full year

  • 歯周病学Ⅱ

    2019.4 - 2019.9   First semester

  • 臨床予備実習

    2019.4 - 2019.9   First semester

  • 歯周病学Ⅰ

    2018.10 - 2019.3   Second semester

  • 臨床実習

    2018.4 - 2019.3   Full year

  • 臨床予備実習

    2018.4 - 2018.9   First semester

  • 歯周病学Ⅱ

    2018.4 - 2018.9   First semester

  • 歯周病学Ⅰ

    2017.10 - 2018.3   Second semester

  • 臨床実習

    2017.4 - 2018.3   Full year

  • 臨床予備見学・シミュレーション実習

    2017.4 - 2017.9   First semester

  • 臨床予備実習

    2017.4 - 2017.9   First semester

  • 基幹教育科目 課題協学A

    2016.10 - 2017.3   Second semester

  • 総合歯科学

    2016.10 - 2017.3   Second semester

  • 学生臨床実習

    2016.4 - 2016.9   First semester

  • 歯周病学Ⅱ

    2016.4 - 2016.9   First semester

  • 臨床予備見学・シミュレーション実習

    2016.4 - 2016.9   First semester

  • 臨床予備実習

    2016.4 - 2016.9   First semester

  • 歯周病学Ⅰ

    2015.10 - 2016.3   Second semester

  • 総合歯科学

    2015.10 - 2016.3   Second semester

  • 学生基礎実習(歯周病学Ⅱ)

    2015.4 - 2015.9   First semester

  • 学生臨床実習

    2015.4 - 2015.9   First semester

  • 歯科総論Ⅲ

    2015.4 - 2015.9   First semester

  • 臨床予備見学・シミュレーション実習

    2015.4 - 2015.9   First semester

  • 臨床予備実習

    2015.4 - 2015.9   First semester

  • 歯周病学Ⅰ

    2014.10 - 2015.3   Second semester

  • 学生臨床実習

    2014.4 - 2014.9   First semester

  • 学生基礎実習

    2014.4 - 2014.9   First semester

  • 歯科総論Ⅲ

    2014.4 - 2014.9   First semester

  • 臨床予備見学・シミュレーション実習

    2014.4 - 2014.9   First semester

  • 歯周病学Ⅰ

    2013.10 - 2014.3   Second semester

  • 学生臨床実習

    2013.4 - 2013.9   First semester

  • 歯科総論Ⅲ

    2013.4 - 2013.9   First semester

  • 学生基礎実習

    2013.4 - 2013.9   First semester

  • PBLチュートリアル

    2012.10 - 2013.3   Second semester

  • 学生臨床実習

    2012.4 - 2012.9   First semester

  • 学生基礎実習

    2012.4 - 2012.9   First semester

  • 歯学総論Ⅲ

    2012.4 - 2012.9   First semester

  • 歯学総論Ⅲ

    2011.10 - 2012.3   Second semester

  • 学生臨床実習

    2011.4 - 2011.9   First semester

  • 学生基礎実習

    2011.4 - 2011.9   First semester

  • 学生臨床実習

    2010.4 - 2010.9   First semester

  • 学生基礎実習

    2010.4 - 2010.9   First semester

  • 学生基礎実習

    2009.10 - 2010.3   Second semester

  • 学生臨床実習

    2009.10 - 2010.3   Second semester

▼display all

FD Participation

  • 2023.8   Role:Participation   Title:令和5年度4部局合同男女共同参画FD

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2023.6   Role:Participation   Title:R6年度科研費獲得セミナー~科研費制度及び研究計画書の書き方~

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2022.6   Role:Participation   Title:科研費申請書ー採択に近づく書き方のコツ

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2022.4   Role:Participation   Title:2022年度CPXの概要と昨年度からの変更点について

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2020.6   Role:Participation   Title:ジャーナルをめぐる現状と論文の投稿・入手について

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2020.4   Role:Participation   Title:CBT問題の作問における注意点ー採択される CBT問題を作成する上でのヒントー

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2019.9   Role:Participation   Title:科研費申請のススメ!〜科学研究費補助金制度と研究計画調書作成時の注意点〜

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2019.3   Role:Participation   Title:2019年度臨床実地試験トライアル説明会

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2018.8   Role:Participation   Title:歯学研究院の研究力分析と研究力強化に向けたScopus/Scival/Pure活用例 BIツールを用いた研究力分析の紹介

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2018.5   Role:Participation   Title:臨床実習御臨床能力試験トライアルの実施に向けて

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2018.3   Role:Participation   Title:東京医科歯科大学における国家試験対策の実践

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2017.11   Role:Participation   Title:ARO次世代医療センターの活用方法

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2016.12   Role:Participation   Title:歯学教育の現状と課題/反グローバル化と国際交流

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2016.6   Role:Participation   Title:国立大学改革プランへの対応・東京医科歯科大学歯学部改革への取り組み

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2016.5   Role:Participation   Title:CBT問題作成ワークショップ

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2016.2   Role:Participation   Title:H28年度課題協学科目FD

    Organizer:University-wide

  • 2015.12   Role:Participation   Title:医学教育改革の動向と歯学研究改革/歯学教育認証評価の必要性

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2015.9   Role:Participation   Title:平成27年度歯学研究院第一回FD

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2015.3   Role:Participation   Title:Comparisions between US and European Dental Schools - finances, research and clinical experience

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2015.2   Role:Participation   Title:誤飲・誤嚥のセミナー

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2014.10   Role:Participation   Title:プロフェッショナリズム教育ー特に卒前教育について、授業を紹介しながらー

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2014.9   Role:Participation   Title:科研費獲得のポイント

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2013.10   Role:Participation   Title:PBLとチューターの役割―昭和大学の学部連携PBLの紹介―

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2012.9   Role:Participation   Title:アクティブラーニング とPBLテュートリアル教育

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2012.9   Role:Participation   Title:PBLチュートリアルにおけるチューター(ファシリテータ)の役割

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2012.1   Role:Participation   Title:日本人歯科医師の海外における活動 ―現状と可能性―

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2011.9   Role:Participation   Title:PBLチュートリアル教育 チューター講習会

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2011.9   Role:Participation   Title:東日本大震災 歯科医療従事者派遣活動報告

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2011.8   Role:Participation   Title:九州大学歯学研究院 FD「カリキュラムプランニングワークショップ」

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2011.1   Role:Participation   Title:昭和大学におけるPBL-チュートリアルの取り組み

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2011.1   Role:Participation   Title:歯学教育を取り巻く環境変化と求められる対応 =歯学教育の改善・充実に関する調査研究協力者会議を中心に=

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2011.1   Role:Participation   Title:歯科保健医療対策の動向

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2010.12   Role:Participation   Title:カリキュラムプランニングの基礎 ―目標・方略・評価―

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2010.12   Role:Participation   Title:学び方を学ぶPBLチュートリアル―高知大学での実践にもとづいて

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2010.3   Role:Participation   Title:QUEST-MAP次期中期目標・計画

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2009.12   Role:Participation   Title:演題:化学物質の安全管理対策

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2009.9   Role:Participation   Title:歯学研究院QUEST-MAPの最終案について

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2009.8   Role:Participation   Title:歯学研究院QUEST-MAPの最終案について

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2009.7   Role:Participation   Title:ニューカッスル大学歯学部を事例とした英国の歯学教育制度の紹介

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2009.4   Role:Participation   Title:歯学研究院のQUEST-MAP(最終版)について

    Organizer:[Undergraduate school/graduate school/graduate faculty]

▼display all

Visiting, concurrent, or part-time lecturers at other universities, institutions, etc.

  • 2023  博多メディカル専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2022  博多メディカル専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2021  博多メディカル専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2020  博多メディカル専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2019  博多メディカル専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2018  博多メディカル専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2017  博多メディカル専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2016  博多メディカル専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2015  博多メディカル専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2014  釜山大学歯学部  Classification:Faculty conurrently holding another post  Domestic/International Classification:Japan 

  • 2014  博多メディカル専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2013  釜山大学歯学部  Classification:Faculty conurrently holding another post  Domestic/International Classification:Japan 

  • 2013  博多メディカル専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2012  博多メディカル専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2010  釜山大学歯学部  Domestic/International Classification:Japan 

  • 2009  福岡医科歯科技術専門学校・歯科衛生士科  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2008  香港大学歯学部  Domestic/International Classification:Japan 

  • 2008  釜山大学歯学部  Domestic/International Classification:Japan 

▼display all

Other educational activity and Special note

  • 2023  Special Affairs  OSCE ステーション6補助

     詳細を見る

    OSCE ステーション6補助

  • 2022  Special Affairs  OSCE タイムキーパー責任者

     詳細を見る

    OSCE タイムキーパー責任者

  • 2021  Special Affairs  OSCE タイムキーパー責任者

     詳細を見る

    OSCE タイムキーパー責任者

  • 2021  Special Affairs  2021年度歯学系臨床実習後臨床能力試験一斉技能試験(CSX)実行責任者

     詳細を見る

    2021年度歯学系臨床実習後臨床能力試験一斉技能試験(CSX)実行責任者

  • 2021  Special Affairs  2021年度一斉技能試験(CSX)認定評価者養成WSチーフタスクフォース

     詳細を見る

    2021年度一斉技能試験(CSX)認定評価者養成WSチーフタスクフォース

  • 2020  Special Affairs  OSCE タイムキーパー責任者

     詳細を見る

    OSCE タイムキーパー責任者

  • 2019  Special Affairs  OSCE タイムキーパー責任者

     詳細を見る

    OSCE タイムキーパー責任者

  • 2018  Special Affairs  OSCE タイムキーパー責任者

     詳細を見る

    OSCE タイムキーパー責任者

  • 2017  Special Affairs  Advanced OSCE実施責任者

     詳細を見る

    Advanced OSCE実施責任者

  • 2017  Special Affairs  OSCE タイムキーパー責任者

     詳細を見る

    OSCE タイムキーパー責任者

  • 2016  Special Affairs  OSCE タイムキーパー責任者

     詳細を見る

    OSCE タイムキーパー責任者

  • 2016  Special Affairs  Advanced OSCE実施責任者

     詳細を見る

    Advanced OSCE実施責任者

  • 2015  Special Affairs  2015年度OSCE実行委員会副委員長補佐実施責任者

     詳細を見る

    2015年度OSCE実行委員会副委員長補佐実施責任者

  • 2015  Special Affairs  Advanced OSCE実施責任者

     詳細を見る

    Advanced OSCE実施責任者

  • 2014  Special Affairs  Advanced OSCE評価者

     詳細を見る

    Advanced OSCE評価者

  • 2014  Special Affairs  2014年度OSCE実行委員会副委員長補佐実施責任者

     詳細を見る

    2014年度OSCE実行委員会副委員長補佐実施責任者

  • 2013  Special Affairs  Advanced OSCE評価者

     詳細を見る

    Advanced OSCE評価者

  • 2013  Special Affairs  平成25年度CBT問題作成ワーキンググループC責任者

     詳細を見る

    平成25年度CBT問題作成ワーキンググループC責任者

  • 2013  Special Affairs  OSCE実行委員会委員・ステーション4内部評価者

     詳細を見る

    OSCE実行委員会委員・ステーション4内部評価者

  • 2012  Special Affairs  OSCE実行委員会委員・ステーション4内部評価者

     詳細を見る

    OSCE実行委員会委員・ステーション4内部評価者

  • 2012  Special Affairs  平成24年度CBT問題作成ワーキンググループC責任者

     詳細を見る

    平成24年度CBT問題作成ワーキンググループC責任者

  • 2011  Special Affairs  平成23年度九州大学病院歯科医師臨床研修指導式講習会

     詳細を見る

    平成23年度九州大学病院歯科医師臨床研修指導式講習会

  • 2011  Special Affairs  九州大学歯学研究院 FD「カリキュラムプランニングワークショップ」参加

     詳細を見る

    九州大学歯学研究院 FD「カリキュラムプランニングワークショップ」参加

  • 2011  Special Affairs  OSCE実行委員会委員・ステーション2総責任者

     詳細を見る

    OSCE実行委員会委員・ステーション2総責任者

  • 2011  Special Affairs  平成23年度第2回共用試験歯学系OSCE評価者養成ワークショップⅠ

     詳細を見る

    平成23年度第2回共用試験歯学系OSCE評価者養成ワークショップⅠ

  • 2010  Special Affairs  平成23年度CBT問題作成

     詳細を見る

    平成23年度CBT問題作成

  • 2010  Special Affairs  OSCE実行委員会補助

     詳細を見る

    OSCE実行委員会補助

  • 2009  Special Affairs  間違い探し問題作成説明会

     詳細を見る

    間違い探し問題作成説明会

  • 2009  Special Affairs  OSCE実行委員会評価者

     詳細を見る

    OSCE実行委員会評価者

  • 2009  Special Affairs  平成22年度CBT問題作成

     詳細を見る

    平成22年度CBT問題作成

  • 2008  Special Affairs  間違い探しを基盤とする洞察力育成医療教育

     詳細を見る

    間違い探しを基盤とする洞察力育成医療教育

  • 2008  Special Affairs  第3回医療系大学e-ラーニング全国交流会

     詳細を見る

    第3回医療系大学e-ラーニング全国交流会

▼display all

Outline of Social Contribution and International Cooperation activities

  • JICA口腔健康科学教育 
    海外研修生外来見学指導
    九州大学病院国際化担当医師

Social Activities

  • 歯周組織再生治療 エムドゲイン VS リグロス

    熊本歯周病勉強会  熊本県歯科医師会会館  2019.2

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 開業医は歯周組織再生剤「リグロス🄬」を導入すべきか?

    歯誠会  福岡県歯科医師会会館  2018.7

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 第9回歯科臨床セミナー:長寿社会における地域歯科医療の貢献

    九州大学病院歯科部門・九州大学歯学会  福岡県歯科医師会会館  2017.3

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • もっと知りたいペリオ-日々進化する医療を知ろう!-

    福岡県歯科衛生士会  福岡県歯科医師会会館  2016.12

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 「九州大学病院の歯科治療紹介」「歯周病と全身疾患の関わり合い」

    主催:若宮ダイヤモンドクラブ 共催:若宮校区ねんりんクラブ  若宮公民館  2011.7

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 福岡市歯科医師会会報(10月号) 「Q&Aお答えします」 歯周組織の再生療法の現状について

    福岡市歯科医師会  2010.10

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Other

  • アメリカ合衆国における歯周治療の実際

    歯誠会  福岡県歯科医師会会館  2008.10

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • これだけは知っておきたい歯周治療の基礎知識

    歯誠会  福岡県歯科医師会会館  2006.3

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

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Media Coverage

  • 「研究プロジェクトの精鋭たち/わが医局のエース」 Newspaper, magazine

    ザ・クインテッセンス  2011.5

     More details

    「研究プロジェクトの精鋭たち/わが医局のエース」

Educational Activities for Highly-Specialized Professionals in Other Countries

  • 2010.5   JICA

    Main countries of student/trainee affiliation:Chile

  • 2009.5   JICA

    Main countries of student/trainee affiliation:Chile

Travel Abroad

  • 2010.7

    Staying countory name 1:Austria   Staying institution name 1:Institute of Molecular Biotechnology of the Austrian Academy of Science (IMBA)

  • 2009.4

    Staying countory name 1:United States   Staying institution name 1:Mount Sinai, School of Medicine

  • 2006.6 - 2007.8

    Staying countory name 1:United States   Staying institution name 1:Indiana University

Specialized clinical area

  • Biology / Medicine, Dentistry and Pharmacy / Dentistry / Periodontal Dentistry

Clinician qualification

  • Specialist

    日本歯周病学会

  • Preceptor

    日本歯周病学会

  • Certifying physician

    日本歯科保存学会

Year of medical license acquisition

  • 1999

Notable Clinical Activities

  • ・海外からの患者受け入れ相談窓口となる国際医療連携担当医師 ・九州大学病院個人情報保護における歯周病科保護業務責任者 ・臨床研究認定歯科医師 ・高度先進医療センター百人部会委員 ・歯学部サマースクール外来見学説明担当教員