九州大学-研究者情報 [讃井彰一 (講師) 九州大学病院口腔機能修復科]

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
キーワード：歯周炎　アメロジェニン　GRP78
2017.04～2022.03.

増殖シグナル制御因子を標的とした歯周組織再生療法の開発
キーワード：歯周病、　再生療法、　増殖因子
2008.04～2010.03.

歯周病と免疫担当細胞の細胞骨格分子との関連性
キーワード：歯周病、　細胞骨格、　Tリンパ球
2005.04～2008.03.

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
2017.04～2022.03, 代表者：讃井彰一.

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
2009.04～2012.03, 代表者：福田隆男, 九州大学大学院歯学研究院口腔機能修復学講座歯周病学分野.

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
2008.04～2012.03, 代表者：讃井彰一, 九州大学大学院歯学研究院口腔機能修復学講座歯周病学分野.

主要著書

1.	讃井彰一, 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, 永末書店, p99-102, 2023.02.
2.	讃井彰一、西村英紀, 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, 日本歯周病学会誌, p100-102, 2019.08.
3.	讃井彰一, 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, 永末書店, p100-102, 2019.02.
4.	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, 「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, 医歯薬出版株式会社, 2013.05.
5.	讃井彰一、前田勝正, 「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」, ザ・クインテッセンス；30 (5), 200-201, 2011.05.
6.	讃井彰一，福井宣規, 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, 医薬の門社, 2003.03.
7.	讃井彰一，福井宣規, DOCK2によるT細胞機能の制御：臨床免疫, 科学評論社, 41巻3号,243-247頁, 2004.03.
8.	讃井彰一，福井宣規, 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, 秀潤社, 22巻11号,1204-1207頁, 2003.08.
9.	讃井彰一，福井宣規，笹月健彦, 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, ニューサイエンス社, 33巻1号,52-54頁, 2002.04.

主要原著論文

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1.	Yamato H, Sanui T, Yotsumoto K, Nakao Y, Watanabe Y, Hayashi C, Aihara R, Iwashita M, Tanaka U, Taketomi T, Fukuda T, Nishimura F., Combined application of geranylgeranylacetone and amelogenin promotes angiogenesis and wound healing in human periodontal ligament cells., Journal of Cellular Biochemistry, doi: 10.1002/jcb.29903., 2021.02.
2.	Yotsumoto K, Sanui T, Tanaka U, Yamato H, Alshargabi R, Shinjo T, Nakao Y, Watanabe Y, Hayashi C, Taketomi T, Fukuda T, Nishimura F, 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., Frontiers in Immunology, doi.org/10.3389/fimmu.2020.00709, 11, 709-709, 2020.03.
3.	Sanui T, Fukuda T, Tanaka U, Toyoda K, Yotsumoto K, Nakao Y, Yamato H, Taketomi T, Nishimura F, Sprouty2 Inhibition Resolves Inflammation in Periodontal Disease and Creates a Suitable Environment for Periodontal Tissue Regeneration., Journal of Cell Biology & Immunology, 1, 101-101, 2017.11.
4.	Terukazu Sanui, Masaaki Takeshita, Takao Fukuda, Urara Tanaka, Rehab Alshargabi, Yoshitomi Aida, Fusanori Nishimura, Roles of serum in innate immune responses of human leukocytes to synthetic lipopeptide, International Immunopharmacology, 10.1016/j.intimp.2017.06.006, 50, 61-68, 2017.09, [URL], 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..
5.	Terukazu Sanui, Masaaki Takeshita, Takao Fukuda, Urara Tanaka, Rehab Alshargabi, Yoshitomi Aida, Fusanori Nishimura, Adhesion attenuates respiratory burst induced by different modes of triggering in resting or LPS-primed neutrophils, Immunobiology, 10.1016/j.imbio.2017.05.001, 222, 8-9, 865-871, 2017.08, [URL], 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..
6.	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, Microarray analysis of the effects of amelogenin on U937 monocytic cells., American Journal of Molecular Biology, in press, 2017.04.
7.	Terukazu Sanui, Masaaki Takeshita, Takao Fukuda, Akira Haraguchi, Yoshitomi Aida, Fusanori Nishimura, Anti-CD14 Antibody-treated Neutrophils Respond to LPS Possible Involvement of CD14 Upregulated by Anti-CD14 Antibody Binding, Immunological Investigations, 10.1080/08820139.2016.1238925, 46, 2, 190-200, 2017.02, [URL], 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..
8.	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, Biological effects of Sprouty2 inhibition in periodontal ligament cells., Journal of Cell Signaling, 10.4172/jcs.1000117, 1, 117, 2016.07.
9.	Terukazu Sanui, Urara Tanaka, Takao Fukuda, Kyousuke Toyoda, Takaharu Taketomi, Ryo Atomura, Kensuke Yamamichi, Fusanori Nishimura, Mutation of Spry2 Induces Proliferation and Differentiation of Osteoblasts but Inhibits Proliferation of Gingival Epithelial Cells, Journal of Cellular Biochemistry, 10.1002/jcb.25014, 116, 4, 628-639, 2015.04, [URL], 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..
10.	讃井彰一, 福田隆男, 田中麗, 豊田敬介, 武富孝治, 西村英紀, Spry2 is a novel therapeutic target for periodontal tissue regeneration through fibroblast growth factor receptor signaling and epidermal growth factor signaling, Receptors & Clinical Investigation, 10.14800/rci.597, e597-e597, 2015.03.
11.	Terukazu Sanui, R. L. Gregory, Analysis of Streptococcus mutans biofilm proteins recognized by salivary immunoglobulin A, Molecular Oral Microbiology, 10.1111/j.1399-302X.2009.00523.x, 24, 5, 361-368, 2009.10, [URL], 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..
12.	Terukazu Sanui, Ayumi Inayoshi, Mayuko Noda, Eiko Iwata, Jens V. Stein, Takehiko Sasazuki, Yoshinori Fukui, DOCK2 regulates Rac activation and cytoskeletal reorganization through interaction with ELMO1, Blood, 10.1182/blood-2003-01-0173, 102, 8, 2948-2950, 2003.10, [URL], 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..
13.	Terukazu Sanui, Ayumi Inayoshi, Mayuko Noda, Eiko Iwata, Masahiro Oike, Takehiko Sasazuki, Yoshinori Fukui, DOCK2 is essential for antigen-induced translocation of TCR and lipid rafts, but not PKC-θ and LFA-1, in T cells, Immunity, 10.1016/S1074-7613(03)00169-9, 19, 1, 119-129, 2003.07, [URL], 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..

主要総説, 論評, 解説, 書評, 報告書等

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1.	讃井彰一, 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, 福岡県歯科医師会「歯界時報」学術レポート, 2022.09.
2.	讃井彰一, 四本かれん, 西村英紀., EMD Science Flash「Emdogain Gelの炎症抑制効果」, ストローマンジャパン, 2020.09.
3.	讃井彰一、西村英紀, 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, 日本歯周病学会誌, 2019.09.
4.	讃井彰一, 四本かれん, 西村英紀., 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, 永末書店, 2019.02.
5.	讃井彰一, 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, 日本歯周病学会誌, doi.org/10.2329/perio.60.117, 2018.09.

主要学会発表等

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1.	讃井彰一, 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, 第61回春季日本歯周病学会学術大会, 2018.06, 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.
2.	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, 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, 第60回春季日本歯周病学会学術大会, 2017.05.
3.	Terukazu Sanui, Hajime Akiyama, Takao Fukuda, Urara Tanaka, Kyosuke Toyoda, Takaharu Taketomi, Fusanori Nishimura, Spry2 Downregulation Shifts Macrophages Toward an M2 Phenotype by Stimulation with Interferon γ and Porphyromonas gingivalis Lipopolysaccharide., 94th General Session & Exhibition of the International Association for Dental Research, 2016.06.
4.	讃井彰一, 福田隆男, 田中麗, 豊田敬介, 山道研介, 西村英紀, Spry2 Downregulation Shifts Macrophages Toward an M2 Phenotype by Stimulation with Interferon γ and Porphyromonas Gingivalis Lipopolysaccharide., 94rd General Session & Exhibition of the International Association for Dental Research, 2016.06.
5.	讃井彰一, Symposium 1: Spry2 is a new therapeutic target for periodontal tissue regeneration., The 63rd Annual Meeting of Japanese Association for Dental Research, 2015.10.
6.	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, The Effects of Spry2 in Osteoblasts and Gingival Epithelial Cells., 93rd General Session & Exhibition of the International Association for Dental Research, 2015.03.
7.	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, Sprouty2 regulates cell proliferation and migration in periodontal ligament cells, 93rd General Session & Exhibition of the International Association for Dental Research, 2015.03.
8.	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, 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., 62nd Annual Meeting of Japanese Association for Dental Research, 2014.12.
9.	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, 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, 第56回秋季日本歯周病学会学術大会, 2013.09.
10.	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, Inhibition of Spry2 decreased EGF receptors in gingival epithelial cells., 10th Asian Pacific Society of Periodontology Meeting, 2013.09.
11.	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, Sprouty2 regulates degradation of EGF receptors in gingival epithelial cells., 2nd meeting of IADR-APR, 2013.08.
12.	Sanui Terukazu, Tanaka Urara, Toyoda Kyosuke, Fukuda Takao, Takaharu Taketomi, Atomura Ryo, Hamachi Takafumi, Maeda Katsumasa, Sprouty2 regulates osteoblastogenesis via Runx2 signaling., 91nd General Session & Exhibition of the IADR, 2013.03.
13.	Terukazu Sanui, Urara Tanaka, Kyosuke Toyoda, Takao Fukuda, Ryo Atomura, Takafumi Hamachi, and Katsumasa Maeda, Inhibition of Sprouty2 Polarizes Macrophages toward M2 Phenotype in Periodontitis, Kyudai Oral Bioscience 2013 —7th International Symposium —, 2013.03, 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..
14.	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, 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, 第22 回日本歯科医学会総会, 2012.11.
15.	Terukazu Sanui, Kyosuke Toyoda, Takao Fukuda, Urara Tanaka, Ryou Atomura, Takafumi Hamachi, Katsumasa Maeda, YB-1 regulates cell proliferation and differentiation in osteoblasts., 98th Annual Meeting American Academy of Periodontology in collaboration with the Japanese Society of Periodontology, 2012.09.
16.	T. SANUI, U. TANAKA, T. FUKUDA, K. TOYODA, T. TAKETOMI, R. ATOMURA, T. HAMACHI, and K. MAEDA, Periodontal Regenerative Effect by Inhibition of Sprouty2 Protein., Pan Europe Region / International Association for Dental Research (PER/IADR）Meeting, 2012.09.
17.	T. SANUI, T. FUKUDA, T. TAKETOMI, T. HAMACHI, and K. MAEDA, Suppression of Sprouty2 Induces Periodontal Tissue Regeneration., The 88th International Association for Dental Research （IADR）, 2010.07.
18.	Terukazu Sanui and Richard L. Gregory, Analysis of Streptococcus mutans Biofilm Proteins Recognized by Salivary IgA., The 87th International Association for Dental Research (IADR), 2009.04.
19.	讃井彰一、笹月健彦、福井宣規, 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, 日本免疫学会, 2002.12.
20.	讃井彰一、福井宣規、橋本修、白井俊一、笹月健彦, リンパ球の運動性を制御する分子の同定, 日本免疫学会, 2001.12.
21.	讃井彰一、福井宣規、大野隆真、笹月健彦, 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, 日本免疫学会, 2000.11.

所属学会名

日本歯科保存学会

日本歯周病学会

日本歯科研究学会（JADR)

国際歯科研究学会（IADR)

日本免疫学会

学協会役員等への就任

2023.04～2025.03, 日本歯周病学会, 運営委員.

2021.04～2023.03, 日本歯周病学会, 運営委員.

2019.04～2021.03, 日本歯周病学会, 運営委員.

2017.04～2019.03, 日本歯周病学会, 運営委員.

2016.04～2029.03, 日本歯周病学会, 評議員.

2015.04～2016.05, 日本歯科保存学会, 編集連絡委員.

2015.04～2016.05, 日本歯周病学会, 編集連絡委員.

学会大会・会議・シンポジウム等における役割

2021.10.24～2021.10.25, The 69rd Annual Meeting of Japanese Association for Dental Research, 準備委員長.

2019.02.10～2019.02.10, 日本歯周病学会第1回佐賀地区臨床研修会, 準備委員長.

2018.05.31～2018.05.31, 日本歯周病学会　若手研究者の集い, 座長.

2017.05.11～2017.05.13, 第60回日本歯周病学会春季学術大会, 準備委員長.

2015.10.30～2015.10.31, The 63rd Annual Meeting of Japanese Association for Dental Research, シンポジスト.

2013.03.08～2013.03.09, Kyudai Oral Bioscience 2013 —7th International Symposium —, シンポジスト.

2009.10.11～2009.10.11, 第５２回秋季日本歯周病学会学術大会, メイン会場責任者.

学会誌・雑誌・著書の編集への参加状況

2015.04～2026.03, 日本歯科保存学会会誌, 国内, 編集連絡委員.

2015.04～2026.03, 日本歯周病学会会誌, 国内, 編集連絡委員.

学術論文等の審査

年度	外国語雑誌査読論文数	合計
2023年度	1	1
2022年度	2	2
2021年度	10	10
2020年度	8	8
2019年度	1	1
2018年度	1	1
2017年度	3	3
2016年度	4	4
2015年度	5	5
2014年度	1	1
2010年度	1	1

海外渡航状況, 海外での教育研究歴

Institute of Molecular Biotechnology of the Austrian Academy of Science (IMBA), Austria, 2010.07～2010.07.

Mount Sinai, School of Medicine, UnitedStatesofAmerica, 2009.04～2009.04.

Indiana University, UnitedStatesofAmerica, 2006.06～2007.08.

第17回（2017年度）日本歯周病学会学術賞, 日本歯周病学会, 2017.12.

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, 財団法人武田科学振興財団, 2017.11.

平成26年度学術研究振興基金助成金, 久留米大学, 2014.04.

2011年度上原記念生命科学財団研究奨励金受賞, 上原記念生命科学財団, 2011.12.

ICPF 2010 Best Paper Award, Co-researcher, International Cleft Palate Foundation, 2010.06.

第64回学会賞優秀発表賞共同研究者, 日本口腔科学会, 2010.06.

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, 財団法人武田科学振興財団, 2009.08.

科学研究費補助金の採択状況(文部科学省、日本学術振興会)

2024年度～2026年度, 基盤研究(B), 代表, 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.

2023年度～2023年度, 基盤研究(B), 代表, 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.

2020年度～2023年度, 基盤研究(C), 代表, 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.

2020年度～2022年度, 基盤研究(C), 分担, 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年度～2023年度, 基盤研究(B), 分担, 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.

2017年度～2019年度, 基盤研究(C), 代表, 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.

2017年度～2019年度, 基盤研究(C), 分担, 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年度～2019年度, 基盤研究(C), 分担, 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.

2016年度～2020年度, 基盤研究(B), 分担, 歯周医学の新展開～歯周炎症とエネルギー代謝の連関.

2014年度～2016年度, 挑戦的萌芽研究, 分担, 歯髄細胞由来TNF誘導因子（DPTIF）受容体の探索研究.

2014年度～2016年度, 基盤研究(C), 分担, 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年度～2016年度, 基盤研究(C), 分担, 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年度～2016年度, 基盤研究(C), 代表, 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.

2012年度～2013年度, 若手研究(B), 代表, 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.

2010年度～2011年度, 若手研究(B), 代表, Sproutyを分子標的薬とした歯周組織再生療法の発明.

2005年度～2007年度, 特別研究員奨励費, 代表, 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.

2008年度～2009年度, 若手研究(スタートアップ), 代表, 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.

寄附金の受入状況

2023年度, 財団法人NSKナカニシ財団, NSKナカニシ財団2023年度研究開発助成.

2023年度, 財団法人小林財団, 令和5年第12回小林財団研究助成.

2017年度, 財団法人武田科学振興財団, 財団法人武田科学振興財団　2017年度医学系研究奨励金.

2014年度, 久留米大学, 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 .

2011年度, 公益財団法人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.

2009年度, 財団法人武田科学振興財団, 財団法人武田科学振興財団　2009年度医学系研究奨励金.

学内資金・基金等への採択状況

2024年度～2025年度, 【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, 分担, 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.

2009年度～2009年度, 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, 代表, 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.


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