Updated on 2024/11/12

Information

 

写真a

 
JIMI EIJIRO
 
Organization
Faculty of Dental Science Department of Dental Science Professor
Faculty of Dental Science OBT Research Center（Concurrent）
School of Dentistry Department of Dentistry（Concurrent）
Graduate School of Dental Science （Concurrent）
Graduate School of Dental Science Department of Dental Science（Concurrent）
Title
Professor
Contact information
メールアドレス
Profile
1991年　九州大学歯学部卒業 1995年　九州大学大学院修了　博士（歯学）号取得 1995年　昭和大学歯学部生化学助手 1998年　ハワードヒューズ医学研究所　研究員 　　　　（イエール大学医学部） 2003年　福岡歯科大学　細胞生理学分野　助教授 2005年　九州歯科大学生命科学講座　生化学分野　教授 2007年　公立大学法人九州歯科大学生命科学講座 　　　　 分子情報生化学分野　教授 2017年　九州大学歯学研究院OBT研究センター長・教授 　　　　 九州大学歯学研究院 口腔細胞工学分野教授（兼担） 2021年　九州大学歯学研究院 副研究院長 （所属等）歯科基礎医学会　常任理事 日本骨代謝学会　評議員 先端歯学国際教育研究ネットワーク副議長 歯科医師国家試験作問委員など 平成30年３月31日にOBT研究センターキックオフシンポジウムを開催 平成31年３月２、３日に第１回KOB・OBT研究センター合同国際シンポジウムを開催 令和元年2月8、9日に第２回KOB・OBT研究センター合同国際シンポジウムを開催 令和２年２月６日に第３回KOB・OBT研究センター合同国際シンポジウムを開催 令和３年２月６日に第４回KOB・OBT研究センター合同国際シンポジウムをオンラインで開催 令和３年11月27-28日に第３回KOB・OBT研究センター合同国際シンポジウムを開催 令和４年10月29-30日に第４回KOB・OBT・DDR研究センター合同国際シンポジウムを開催
External link

Research Areas

  • Life Science / Oral biological science

Degree

  • DDS.,Ph.D

Research History

  • Kyushu University Faculty of Dental Science Professor

    2021.4 - Present

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    Country：Japan

  • Kyushu University 1Laboratory of Molecular and Cellular Biochemistry, Division of Oral Biological Sciences, Faculty of Dental Science Professor

    2017.5 - Present

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    Country：Japan

  • OBT Research Center, Faculty of Dental Science OBT Research Center, Faculty of Dental Science, Professor

    2017.4 - Present

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  • Kyushu Dental College Division of Molecular Signaling and Biochemistry, Department of Health Improvement, Professor

    2005.6 - 2017.3

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    Country：Japan

  • Fukuoka Dental College Department of Physiological Science and Molecular Biology, Section of Cellular Physiology Associate Professor (as old post name)

    2003.3 - 2005.5

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    Country：Japan

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  • Yale University, School of Medicine Section of Immunobiology Research Associate

    1998.11 - 2003.2

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    Country：United States

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  • Showa University Research Assistant

    1995.4 - 2000.10

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    Country：Japan

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Education

  • Kyushu University

    1991.4 - 1995.3

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    Country： Japan

  • Kyushu University   School of Dentistry

    1985.4 - 1991.3

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    Country： Japan

Research Interests・Research Keywords

  • Research theme：Elucidation of the molecular basis of bone metabolism regulation by NF-κB and its application to new therapeutic strategies

    Keyword：NF-κB, Bone metabolism, Osteoclasts

    Research period： 2024.9 - 2028.3

  • Research theme：Elucidation of the mechanism of NF-κB activation by female hormone deficiency and the control of bone and energy metabolism

    Keyword：NF-κB, Menopause, Bone loss, Weight gain

    Research period： 2024.4 - 2027.3

  • Research theme：Elucidation of a new bone metabolism regulation mechanism by epithelial cells

    Keyword：epithelial cells, bone metabolism

    Research period： 2023.4 - 2024.4

  • Research theme：Elucidation of new regulatory mechanism of protein deamidation and functional analysis using oral cancer cells

    Keyword：deamidation

    Research period： 2021.10 - 2023.3

  • Research theme：Elucidation of essential common molecular mechanisms that control postmenopausal osteoporosis and weight gain and development of therapeutic strategies

    Keyword：postmenopausal osteoporosis, weight gain

    Research period： 2021.4 - 2021.6

  • Research theme：Bone's function as a new sensor for emotional and immunological health

    Keyword：emotion, immunology, bone, NF-kB

    Research period： 2020.10 - 2021.6

  • Research theme：Morphogenesis and differentiation by the epithelial-mesenchymal interaction

    Keyword：p130Cas, tooth, salivary gland

    Research period： 2018.4 - 2025.3

  • Research theme：Signaling mechanism of transcription factor NF-kB and its functional analysis

    Keyword：NF-kB, metabolism

    Research period： 2014.4 - 2025.3

  • Research theme：The molecular mechanism of bone invasion by oral squamous cell carcinoma

    Keyword：oral squamous cell carcinoma, bone invasion

    Research period： 2003.4 - 2022.3

  • Research theme：The role of transcription factor NF-kB on bone metabolism

    Keyword：transcription factor, bone metabolism

    Research period： 1991.4 - 2027.4

Awards

  • 第33回日本骨代謝学会学術賞

    2016.8   日本骨代謝学会  

  • ライオン学術賞

    2015.9   日本歯科基礎医学会  

  • 第22回日本骨代謝学会優秀演題賞「骨形成」

    2003.6   日本骨代謝学会  

  • Young Investigator Award

    1997.9  

  • 第８回　歯科基礎医学会賞

    1996.9  

Papers

  • Activation of NF-κB signaling regulates ovariectomy-induced bone loss and weight gain

    Huang, F; Gao, J; Li, AA; Mizokami, A; Matsuda, M; Aoki, K; Katagiri, T; Kawakubo-Yasukochi, T; Jimi, E

    BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE   1870 ( 7 )   167320   2024.10   （ ISSN:0925-4439 eISSN:1879-260X ）

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    Language：English   Publisher：Biochimica et Biophysica Acta - Molecular Basis of Disease  

    Postmenopausal women experience bone loss and weight gain. To date, crosstalk between estrogen receptor signals and nuclear factor-κB (NF-κB) has been reported, and estrogen depletion enhances bone resorption by osteoclasts via NF-κB activation. However, it is unclear when and in which tissues NF-κB is activated after menopause, and how NF-κB acts as a common signaling molecule for postmenopausal weight gain and bone loss. Therefore, we examined the role of NF-κB in bone and energy metabolism following menopause. NF-κB reporter mice, which can be used to measure NF-κB activation in vivo, were ovariectomized (OVX) and the luminescence intensity after OVX increased in the metaphyses of the long bones and perigonadal white adipose tissue, but not in the other tissues. OVX was performed on wild-type (WT) and p65 mutant knock-in (S534A) mice, whose mutation enhances the transcriptional activity of NF-κB. Weight gain with worsening glucose tolerance was significant in S534A mice after OVX compared with those of WT mice. The bone density of the sham group in WT or S534A mice did not change, whereas in the S534A-OVX group it significantly decreased due to the suppression of bone formation and increase in bone marrow adipocytes. Disulfiram, an anti-alcoholic drug, suppressed OVX-induced activation of NF-κB in the metaphyses of long bones and white adipose tissue (WAT), as well as weight gain and bone loss. Overall, the activation of NF-κB in the metaphyses of long bones and WAT after OVX regulates post-OVX weight gain and bone loss.

    DOI： 10.1016/j.bbadis.2024.167320

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  • Phosphorylation of Serine 536 of p65(RelA) Downregulates Inflammatory Responses

    Aoki, T; Gao, J; Li, A; Huang, F; Tu, YR; Wu, W; Matsuda, M; Kiyoshima, T; Nishimura, F; Jimi, E

    INFLAMMATION   2024.9   （ ISSN:0360-3997 eISSN:1573-2576 ）

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    Language：English   Publisher：Inflammation  

    Nuclear factor-κB (NF-κB) is a transcription factor that regulates the expression of various genes involved in inflammatory diseases and immune responses. Recently, a novel transcriptional regulatory mechanism of NF-κB involving the phosphorylation of serine 536 (534 in mice; S534) of its p65 subunit was reported; however, further research is required to elucidate the physiological role of S534 phosphorylation. Therefore, we generated S534A knock-in (KI) mice, in which the S534 of p65 was substituted with alanine. Similar to the wild-type (WT) mice, S534A KI mice developed normally. After stimulation with tumor necrosis factor α (TNFα), mouse embryonic fibroblasts (MEFs) derived from S534A KI mice exhibited increased target gene expression compared with that in the WT MEFs, which was induced by long-term binding of p65 to DNA. According to comprehensive gene expression analysis after stimulation with TNFα, the expression of genes p65ted to inflammatory and immune responses was increased, and the expression of genes p65ted to lipolysis was decreased in S534A KI MEFs. Analyses of a periodontal disease model established using WT and S534A KI mice revealed that alveolar bone resorption was enhanced in S534A KI mice owing to an increase in the number of osteoclasts, which was not attributed to the differentiation of osteoclast precursor cells but to an increased expression of interleukin-1β and receptor activator of NF-κB ligand in the periodontal tissue. Hence, phosphorylation of S536 negatively regulates inflammatory responses in vitro and in vivo.

    DOI： 10.1007/s10753-024-02140-0

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  • Nuclear factor- K B p65 subunit determines the fate of aging epithelial cells

    Gao, T; Kawabata, Y; Kiyoshima, T; Jimi, E

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   722   150143   2024.8   （ ISSN:0006-291X eISSN:1090-2104 ）

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    Language：English   Publisher：Biochemical and Biophysical Research Communications  

    Nuclear factor (NF)-κB signaling is not only important for the immune and inflammatory responses but also for the normal development of epithelial cells, such as those in the skin and tooth. Here, we generated epithelial cell-specific p65-deficient (p65Δepi−/−) mice to analyze the roles of NF-κB signaling in epithelial cell developent. Notably, p65Δepi−/− mice exhibited no abnormalities in their appearance compared to the control (p65flox/flox) littermates. Furthermore, no major changes were observed in the skin, hair growth, and shape and color of the incisors and molars. However, 65 % of p65Δepi−/− mice exhibited corneal thickening after 8 weeks of age, and 30 % of p65Δepi−/− mice exhibited hair growth from the mandibular incisors around 24 weeks of age. No hair growth was observed at 36 and 42 weeks of age. However, micro-computed tomography images revealed a large cavity below the mandibular incisors extending to the root of the incisor. Histological analysis revealed that the cavity was occupied by a connective tissue containing hair-like structures with many dark brown granules that disappeared after melanin bleaching, confirming the presence of hair. Although inflammatory cells were also observed near the eruption site of the incisor teeth of p65Δepi−/− mice, no major disturbance was observed in the arrangement of enamel epithelial cells. Overall, these results highlight the role of p65 in the maintenance of epithelial cell homeostasis during aging.

    DOI： 10.1016/j.bbrc.2024.150143

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  • Inhibition of the ATG4-LC3 pathway suppressed osteoclast maturation. Reviewed International journal

    #Hiura F, Kawabata Y, #Aoki T, Mizokami A, Jimi E.

    Biochem Biophys Res Commun.   2023.12

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

    DOI： doi: 10.1016/j.bbrc.2022.09.065.

    Repository Public URL： https://hdl.handle.net/2324/7178663

  • The G protein-coupled receptor GPRC5C is a saccharide sensor with a novel 'off' response

    Kawabata, Y; Takai, S; Sanematsu, K; Iwata, S; Kawabata, F; Kanematsu, T; Jimi, E; Shigemura, N

    FEBS LETTERS   597 ( 15 )   2006 - 2016   2023.8   （ ISSN:0014-5793 eISSN:1873-3468 ）

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    Language：English   Publisher：FEBS Letters  

    GPRC5C is an orphan G protein-coupled receptor (GPCR) that belongs to the class C GPCR family. Although GPRC5C is expressed in various organs, its function and ligand are still undetermined. We found that GPRC5C is expressed in mouse taste cells, enterocytes, and pancreatic α-cells. In functional imaging assays, HEK293 cells heterologously expressing GPRC5C and the chimeric G protein α subunit Gα16-gust44 showed robust intracellular Ca2+ increases in response to monosaccharides, disaccharides, and a sugar alcohol, but not an artificial sweetener or sweet-tasting amino acid. Notably, Ca2+ increases occurred after washout, not during stimulation. Our findings suggest that GPRC5C has receptor properties which lead to novel ‘off’ responses to saccharide detachment and may work as an internal or external chemosensor specifically tuned to natural sugars.

    DOI： 10.1002/1873-3468.14695

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  • Wnt7b expressed by hypertrophic chondrocytes is a stimulatory factor for endochondral ossification that is regulated by Smad4 activity

    Tsukamoto, S; Kuratani, M; Tanaka, S; Jimi, E; Oda, H; Katagiri, T

    DEVELOPMENT   150 ( 15 )   2023.8   （ ISSN:0950-1991 eISSN:1477-9129 ）

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    Language：English   Publisher：Development (Cambridge)  

    Endochondral ossification contributes to longitudinal skeletal growth. Osteoblasts, which are bone-forming cells, appear close to terminally differentiated hypertrophic chondrocytes during endochondral ossification. We established mice with conditional knockout (cKO) of Smad4, an essential co-activator for transforming growth factor β family signaling. The mice showed a marked increase in bone volume in the metaphysis as a result of increased bone formation by osteoblasts, in which β-catenin, an effector of canonical Wnt signaling, accumulated. We identified Wnt7b as a factor with increased expression in growth plate cartilage in Smad4 cKO mice. Wnt7b mRNA was expressed in differentiated chondrocytes and suppressed by BMP4 stimulation. Ablation of Wnt7b blunted the increase in bone in adult Smad4 cKO mice and reduced skeletal growth in juvenile mice. Overall, we conclude that Wnt7b is a crucial factor secreted from hypertrophic chondrocytes to initiate endochondral ossification. These results suggest that Smad4-dependent BMP signaling regulates the Wnt7b–β-catenin axis during endochondral ossification.

    DOI： 10.1242/dev.201734

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  • Inhibition of non-canonical NF-kB signaling suppresses periodontal inflammation and bone loss

    Aoki Tsukasa, Hiura Fumitaka, Li Aonan, Yang Nan, Takakura Nana, Mukai Satoru, Matsuda Miho, Nishimura Fusanori, Jimi Eijiro

    Frontiers in Immunology   14   1179007   2023.4   （ eISSN:16643224 ）

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    Periodontal disease is an infectious disease that affects many people worldwide. Disease progression destroys the alveolar bone and causes tooth loss. We have previously shown that alymphoplasia (aly/aly) mice harboring a loss-of-function mutation in the map3k14 gene, which is involved in p100 to p52 processing of the alternative NF-κB pathway, exhibited mild osteopetrosis due to decreased number of osteoclasts, suggesting the alternative NF-κB pathway as a potential drug target for the amelioration of bone disease. In the present study, wild-type (WT) and aly/aly mice were subjected to silk ligation to establish a periodontitis model. Alveolar bone resorption was suppressed in aly/aly mice by decreased numbers of osteoclasts in the alveolar bone in comparison to WT mice. Furthermore, the expression of receptor activator of NF-κB ligand (RANKL) and TNFα (cytokines involved in osteoclast induction in periligative gingival tissue) was decreased. When primary osteoblasts (POBs) and bone marrow cells (BMCs) derived from WT and aly/aly mice were prepared and co-cultured, osteoclasts were induced from WT-derived BMCs, regardless of the origin of the POBs, but hardly formed from aly/aly mouse-derived BMCs. Furthermore, the local administration of an NIK inhibitor, Cpd33, inhibited osteoclast formation and thereby inhibited alveolar bone resorption in the periodontitis model. Therefore, the NIK-mediated NF-κB alternative pathway can be a therapeutic target for periodontal disease.

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  • Inhibition of non-canonical NF-κB signaling suppresses periodontal inflammation and bone loss

    Aoki, T; Hiura, F; Li, AA; Yang, N; Takakura-Hino, N; Mukai, S; Matsuda, M; Nishimura, F; Jimi, E

    FRONTIERS IN IMMUNOLOGY   14   1179007   2023.4   （ ISSN:1664-3224 ）

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    Language：English   Publisher：Frontiers in Immunology  

    Periodontal disease is an infectious disease that affects many people worldwide. Disease progression destroys the alveolar bone and causes tooth loss. We have previously shown that alymphoplasia (aly/aly) mice harboring a loss-of-function mutation in the map3k14 gene, which is involved in p100 to p52 processing of the alternative NF-κB pathway, exhibited mild osteopetrosis due to decreased number of osteoclasts, suggesting the alternative NF-κB pathway as a potential drug target for the amelioration of bone disease. In the present study, wild-type (WT) and aly/aly mice were subjected to silk ligation to establish a periodontitis model. Alveolar bone resorption was suppressed in aly/aly mice by decreased numbers of osteoclasts in the alveolar bone in comparison to WT mice. Furthermore, the expression of receptor activator of NF-κB ligand (RANKL) and TNFα (cytokines involved in osteoclast induction in periligative gingival tissue) was decreased. When primary osteoblasts (POBs) and bone marrow cells (BMCs) derived from WT and aly/aly mice were prepared and co-cultured, osteoclasts were induced from WT-derived BMCs, regardless of the origin of the POBs, but hardly formed from aly/aly mouse-derived BMCs. Furthermore, the local administration of an NIK inhibitor, Cpd33, inhibited osteoclast formation and thereby inhibited alveolar bone resorption in the periodontitis model. Therefore, the NIK-mediated NF-κB alternative pathway can be a therapeutic target for periodontal disease.

    DOI： 10.3389/fimmu.2023.1179007

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  • Inhibition of non-canonical NF-B signaling suppresses periodontal inflammation and bone loss. Invited Reviewed International journal

    #Aoki T, #Hiura F, #Li A, #Yang N, Takakura-Hino N, Mukai S, ＠Matsuda M, ＠Nishimura F, ＠Jimi E.

    2023.4

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    DOI： 10.3389/fimmu.2023.1179007.

    Repository Public URL： https://hdl.handle.net/2324/7172190

  • p130Cas is required for androgen-dependent postnatal development regulation of submandibular glands. Reviewed International journal

    Sci Rep.   2023.3

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

    DOI： 10.1038/s41598-023-32390-1.

    Repository Public URL： https://hdl.handle.net/2324/7178662

  • Id4 modulates salivary gland homeostasis and its expression is downregulated in IgG4-related disease via miR-486-5p. Reviewed International journal

    @Hayashi Y, #Kimura S, Yano E, @Yoshimoto S, Saeki A, Yasukochi A, Hatakeyama Y, Moriyama M, Nakamura S, Jimi E, Kawakubo-Yasukochi T.

    Biochim Biophys Acta Mol Cell Res.   2023.2

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

    DOI： 10.1016/j.bbamcr.2022.119404.

  • Critical Roles of NF-κB Signaling Molecules in Bone Metabolism Revealed by Genetic Mutations in Osteopetrosis

    Jimi, E; Katagiri, T

    INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES   23 ( 14 )   2022.7   （ ISSN:16616596 eISSN:1422-0067 ）

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    Language：English   Publisher：International Journal of Molecular Sciences  

    The nuclear factor-κB (NF-κB) transcription factor family consists of five related proteins, RelA (p65), c-Rel, RelB, p50/p105 (NF-κB1), and p52/p100 (NF-κB2). These proteins are important not only for inflammation and the immune response but also for bone metabolism. Activation of NF-κB occurs via the classic and alternative pathways. Inflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β, activate the former, and cytokines involved in lymph node formation, such as receptor activator of NF-κB ligand (RANKL) and CD40L, activate the latter. p50 and p52 double-knockout mice revealed severe osteopetrosis due to the total lack of osteoclasts, which are specialized cells for bone resorption. This finding suggests that the activation of NF-κB is required for osteoclast differentiation. The NF-κB signaling pathway is controlled by various regulators, including NF-κB essential modulator (NEMO), which is encoded by the IKBKG gene. In recent years, mutant forms of the IKBKG gene have been reported as causative genes of osteopetrosis, lymphedema, hypohidrotic ectodermal dysplasia, and immunodeficiency (OL-EDA-ID). In addition, a mutation in the RELA gene, encoding RelA, has been reported for the first time in newborns with high neonatal bone mass. Osteopetrosis is characterized by a diffuse increase in bone mass, ranging from a lethal form observed in newborns to an asymptomatic form that appears in adulthood. This review describes the genetic mutations in NF-κB signaling molecules that have been identified in patients with osteopetrosis.

    DOI： 10.3390/ijms23147995

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  • RANKL elevation activates the NIK/NF-κB pathway, inducing obesity in ovariectomized mice. Invited Reviewed International journal

    2022.4

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

    DOI： 10.1530/JOE-21-0424

    Repository Public URL： https://hdl.handle.net/2324/7178665

  • Phospholipase C-related catalytically inactive protein acts as a positive regulator for insulin signalling in adipocytes. Reviewed International journal

    Gao J, Mizokami A, Takeuchi H, Li A, Huang F, Nagano H, Kanematsu T, Jimi E, Hirata M.

    J Cell Sci. 2022 135(1):jcs258584.   2022.4

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    DOI： 10.1242/jcs.258584.

  • Phospholipase C-related but catalytically inactive protein acts as a positive regulator of insulin signalling in adipocytes

    Gao, J; Mizokami, A; Takeuchi, H; Li, AN; Huang, F; Nagano, H; Kanematsu, T; Jimi, E; Hirata, M

    JOURNAL OF CELL SCIENCE   135 ( 1 )   2022.1   （ ISSN:0021-9533 eISSN:1477-9137 ）

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    Language：English   Publisher：Journal of Cell Science  

    Insulin signalling is tightly controlled by various factors, but the exact molecular mechanism remains incompletely understood. We have previously reported that phospholipase C-related but catalytically inactive protein (PRIP; used here to refer to both PRIP-1 and PRIP-2, also known as PLCL1 and PLCL2, respectively) interacts with Akt1, the central molecule in insulin signalling. Here, we investigated whether PRIP is involved in the regulation of insulin signalling in adipocytes. We found that insulin signalling, including insulin-stimulated phosphorylation of the insulin receptor (IR), insulin receptor substrate-1 (IRS-1) and Akt, and glucose uptake were impaired in adipocytes from PRIP double-knockout (PRIP-KO) mice compared with those from wild-type (WT) mice. The amount of IR expressed on the cell surface was decreased in PRIP-KO adipocytes. Immunoprecipitation assays showed that PRIP interacted with IR. The reduced cell surface IR in PRIP-KO adipocytes was comparable with that in WT cells when Rab5 (Rab5a, -5b and -5c) expression was silenced using specific siRNA. In contrast, the dephosphorylation of IRS-1 at serine residues, some of which have been reported to be involved in the internalisation of IR, was impaired in cells from PRIP-KO mice. These results suggest that PRIP facilitates insulin signalling by modulating the internalisation of IR in adipocytes.

    DOI： 10.1242/jcs.258584

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  • RAF1-MEK/ERK pathway-dependent ARL4C expression promotes ameloblastoma cell proliferation and osteoclast formation

    Fujii, S; Ishibashi, T; Kokura, M; Fujimoto, T; Matsumoto, S; Shidara, S; Kurppa, KJ; Pape, J; Caton, J; Morgan, PR; Heikinheimo, K; Kikuchi, A; Jimi, E; Kiyoshima, T

    JOURNAL OF PATHOLOGY   256 ( 1 )   119 - 133   2022.1   （ ISSN:0022-3417 eISSN:1096-9896 ）

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    Language：English   Publisher：Journal of Pathology  

    Ameloblastoma is an odontogenic neoplasm characterized by slow intraosseous growth with progressive jaw resorption. Recent reports have revealed that ameloblastoma harbours an oncogenic BRAFV600E mutation with mitogen-activated protein kinase (MAPK) pathway activation and described cases of ameloblastoma harbouring a BRAFV600E mutation in which patients were successfully treated with a BRAF inhibitor. Therefore, the MAPK pathway may be involved in the development of ameloblastoma; however, the precise mechanism by which it induces ameloblastoma is unclear. The expression of ADP-ribosylation factor (ARF)-like 4c (ARL4C), induced by a combination of the EGF–MAPK pathway and Wnt/β-catenin signalling, has been shown to induce epithelial morphogenesis. It was also reported that the overexpression of ARL4C, due to alterations in the EGF/RAS–MAPK pathway and Wnt/β-catenin signalling, promotes tumourigenesis. However, the roles of ARL4C in ameloblastoma are unknown. We investigated the involvement of ARL4C in the development of ameloblastoma. In immunohistochemical analyses of tissue specimens obtained from 38 ameloblastoma patients, ARL4C was hardly detected in non-tumour regions but tumours frequently showed strong expression of ARL4C, along with the expression of both BRAFV600E and RAF1 (also known as C-RAF). Loss-of-function experiments using inhibitors or siRNAs revealed that ARL4C elevation depended on the RAF1–MEK/ERK pathway in ameloblastoma cells. It was also shown that the RAF1–ARL4C and BRAFV600E–MEK/ERK pathways promoted cell proliferation independently. ARL4C-depleted tumour cells (generated by knockdown or knockout) exhibited decreased proliferation and migration capabilities. Finally, when ameloblastoma cells were co-cultured with mouse bone marrow cells and primary osteoblasts, ameloblastoma cells induced osteoclast formation. ARL4C elevation in ameloblastoma further promoted its formation capabilities through the increased RANKL expression of mouse bone marrow cells and/or primary osteoblasts. These results suggest that the RAF1–MEK/ERK–ARL4C axis, which may function in cooperation with the BRAFV600E–MEK/ERK pathway, promotes ameloblastoma development. © 2021 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

    DOI： 10.1002/path.5814

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  • 妊娠母体栄養がもたらす産仔の肝グリコーゲン分解異常と オステオカルシンによる回避

    安河内（川久保） 友世, 矢野 恵奈, 木村 宗惟, 溝上 顕子, 林 慶和, 安河内 篤, 中村 誠司, 自見 英治郎, 平田 雅人

    DOHaD研究   10 ( 2 )   42   2022   （ ISSN:21872562 eISSN:21872597 ）

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    Language：Japanese   Publisher：一般社団法人 日本DOHaD学会  

    DOI： 10.51067/dohad.10.2_42

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  • Deletion of epithelial cell-specific p130Cas impairs the maturation stage of amelogenesis. Reviewed International journal

    #Inoue A, @Kiyoshima T, @Yoshizaki K, Nakatomi C, Nakatomi M, Ohshima H, Shin M, @Gao J, Tsuru K, Okabe K, Nakamura I, Honda H, @Matsuda M, @Takahashi I, @Jimi E.

    Bone   154   116210   2021.11

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

    DOI： 10.1016/j.bone.2021.116210

    Repository Public URL： https://hdl.handle.net/2324/7178667

  • Bone morphogenetic protein induces bone invasion of melanoma by epithelial-mesenchymal transition via the Smad1/5 signaling pathway. Reviewed International journal

    Gao J, Muroya R, Huang F, Nagata K, Shin M, Nagano R, Tajiri Y, Fujii S, Yamaza T, Aoki K, Tamura Y, Inoue M, Chishaki S, Kukita T, Okabe K, Matsuda M, Mori Y, Kiyoshima T, Jimi E.

    Lab Invest.   101   1475 - 1483   2021.11

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

    DOI： 10.1038/s41374-021-00661-y.

  • Hepatic glycogenolysis is determined by maternal high-calorie diet via methylation of Pygl and this is modified by osteocalcin administration in mice. Reviewed International journal

    Kawakubo-Yasukochi T, Yano E, Kimura S, Nishinakagawa T, Mizokami A, Hayashi Y, Hatakeyama Y, Ohe K, Yasukochi A, Nakamura S, Jimi E, Hirata M.

    Mol Metab.   2021.10

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

    DOI： 10.1016/j.molmet.2021.101360.

  • RAF1-MEK/ERK pathway-dependent ARL4C expression promotes ameloblastoma cell proliferation and osteoclast formation. Reviewed International journal

    @Fujii S, Ishibashi T, @Kokura M, Fujimoto T, Matsumoto S, Shidara S, Kurppa KJ, Pape J, Caton J, Morgan PR, Heikinheimo K, Kikuchi A, @Jimi E, @Kiyoshima T.

    J Pathol.   2021.10

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

    DOI： 10.1002/path.5814.

  • Volume-regulated chloride channel regulates cell proliferation and is involved in the possible interaction between TMEM16A and LRRC8A in human metastatic oral squamous cell carcinoma cells. Reviewed International journal

    Yoshimoto S, Matsuda M, Kato K, Jimi E, Takeuchi H, Nakano S, Kajioka S, Matsuzaki E, Hirofuji T, Inoue R, Hirata M, Morita H.

    Eur J Pharmacol.   895   173881   2021.3

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

    DOI： 10.1016/j.ejphar.2021.173881.

  • Adipocyte-specific GPRC6A ablation promotes diet-induced obesity by inhibiting lipolysis. Reviewed International journal

    Mukai S, Mizokami A, Otani T, Sano T, Matsuda M, Chishaki S, Gao, Kawakubo-Yasukochi T, Tang R, Kanematsu T, Takeuchi H, Jimi E, Hirata M.

    J Biol Chem.   296   2021.1

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

    DOI： doi: 10.1016/j.jbc.2021.100274.

  • A small nuclear acidic protein (MTI-II, Zn2+-binding protein, parathymosin) attenuates TNF-α inhibition of BMP-induced osteogenesis by enhancing accessibility of the Smad4-NF-κB p65 complex to Smad binding element. Invited Reviewed International journal

    2020.4

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

    Pro-inflammatory cytokines prevent bone regeneration in vivo and activation of nuclear factor-κB (NF-κB) signaling has been proposed to lead to suppression of bone morphogenetic protein (BMP)-induced osteogenesis via direct binding of p65 to Smad4 in vitro. Application of a small nuclear acidic protein (MTI-II) and its delivered peptide, MPAID (MTI-II peptide anti-inflammatory drug) has been described to elicit therapeutic potential via strong anti-inflammatory action following the physical association of MTI-II and MPAID with p65. However, it is unclear whether MTI-II attenuates tumor necrosis factor (TNF)-α inhibition of BMP-induced osteogenesis. Herein, we found that TNF-α-mediated suppression of responses associated with BMP4-induced osteogenesis, including expression of the osteocalcin encoding gene Ocn, Smad binding element (SBE)-dependent luciferase activity, alkaline phosphatase activity, and alizarin red S staining were largely restored by MTI-II and MPAID in MC3T3-E1 cells. Mechanistically, MTI-II and MPAID did not inhibit nuclear translocation of p65 or disassociate Smad4 from p65. Further, results from chromatin immunoprecipitation (ChIP) analyses revealed that Smad4 enrichment in cells over-expressing MTI-II and treated with TNF-α was equivalent to that in cells without TNF-α treatment. Alternatively, Smad4 enrichment was considerably decreased following TNF-α treatment in control cells. Moreover, p65 enrichment in the Id-1 promoter SBE was detected only when cells over-expressing MTI-II were stimulated with TNF-α. Overall, our study concludes that MTI-II restored TNF-α-inhibited suppression of BMP-Smad-induced osteogenic differentiation by enhancing accessibility of the Smad4-p65 complex to the SBE rather than by liberating Smad4 from p65.

    DOI： doi: 10.1007/s11010-020-03734-6

  • A novel inhibitor of NF-κB-inducing kinase prevents bone loss by inhibiting osteoclastic bone resorption in ovariectomized mice. Invited Reviewed International journal

    2020.3

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

    Musculoskeletal diseases and disorders, including osteoporosis and rheumatoid arthritis are diseases that threaten a healthy life expectancy, and in order to extend the healthy life expectancy of elderly people, it is important to prevent bone and joint diseases and disorders. We previously reported that alymphoplasia (aly/aly) mice, which have a loss-of-function mutation in the Nik gene involved in the processing of p100 to p52 in the alternative NF-κB pathway, show mild osteopetrosis with a decrease in the osteoclast number, suggesting that the alternative NF-κB pathway is a potential drug target for ameliorating bone diseases. Recently, the novel NF-κB-inducing kinase (NIK)-specific inhibitor compound 33 (Cpd33) was developed, and we examined its effect on osteoclastic bone resorption in vitro and in vivo. Cpd33 inhibited the receptor activator of NF-κB ligand (RANKL)-induced osteoclastogenesis accompanied by a decrease in the expression of nfatc1, dc-stamp, and cathepsin K, markers of osteoclast differentiation, without affecting the cell viability, in a dose-dependent manner. Cdp33 specifically suppressed the RANKL-induced processing of p100 to p52 but not the phosphorylation of p65 or the degradation or resynthesis of IκBα in osteoclast precursors. Cpd33 also suppressed the bone-resorbing activity in mature osteoclasts. Furthermore, Cdp33 treatment prevented bone loss by suppressing the osteoclast formation without affecting the osteoblastic bone formation in ovariectomized mice. Taken together, NIK inhibitors may be a new option for patients with a reduced response to conventional pharmacotherapy or who have serious side effects.

    DOI： doi: 10.1016/j.bone.2020.115316.

  • p130Cas induces bone invasion by oral squamous cell carcinoma by regulating tumor epithelial-mesenchymal transition and cell proliferation. Reviewed International journal

    Yaginuma T, Gao J, Nagata K, Muroya R, Fei H, Nagano H, Chishaki S, Matsubara T, Kokabu S, Matsuo K, Kiyoshima T, Yoshioka I, Jimi E.

    Carcinogenesis   2020.1

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

    DOI： 10.1093/carcin/bgaa007.

  • Kif1c regulates osteoclastic bone resorption as a downstream molecule of p130Cas. Reviewed International journal

    Kobayakawa M, Matsubara T, Mizokami A, Hiura F, Takakura N, Kokabu S, Matsuda M, Yasuda H, Nakamura I, Takei Y, Honda H, Hosokawa R, Jimi E.

    Cell Biochem Funct.   2019.12

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

    DOI： doi: 10.1002/cbf.3476.

  • GLP-1 signaling is required for improvement of glucose tolerance by osteocalcin. Reviewed International journal

    Mizokami A, Mukai S, Gao J, Kawakubo-Yasukochi T, Otani T, Takeuchi H, Jimi E, Hirata M.

    J Endocrinol.   2019.11

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  • Bif-1/Endophilin B1/SH3GLB1 regulates bone homeostasis. Reviewed International journal

    Touyama K, Khan M, Aoki K, Matsuda M, Hiura F, Takakura N, Matsubara T, Harada Y, Hirohashi Y, Tamura Y, Gao J, Mori K, Kokabu S, Yasuda H, Fujita Y, Watanabe K, Takahashi Y, Maki K, Jimi E.

    J Cell Biochem   120 ( 11 )   18793 - 18804   2019.11

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

    DOI： doi: 10.1002/jcb.29193.

  • Constitutive activation of the alternative NF-κB pathway disturbs endochondral ossification. Reviewed International journal

    121   29 - 41   2019.4

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

    Endochondral ossification is important for skeletal development. Recent findings indicate that the p65 (RelA) subunit, a main subunit of the classical nuclear factor-κB (NF-κB) pathway, plays essential roles in chondrocyte differentiation. Although several groups have reported that the alternative NF-κB pathway also regulates bone homeostasis, the role of the alternative NF-κB pathway in chondrocyte development is still unclear. Here, we analyzed the in vivo function of the alternative pathway on endochondral ossification using p100-deficient (p100-/-) mice, which carry a homozygous deletion of the COOH-terminal ankyrin repeats of p100 but still express functional p52 protein. The alternative pathway was activated during the periarticular stage in wild-type mice. p100-/- mice exhibited dwarfism, and histological analysis of the growth plate revealed abnormal arrangement of chondrocyte columns and a narrowed hypertrophic zone. Consistent with these observations, the expression of hypertrophic chondrocyte markers, type X collagen (ColX) or matrix metalloproteinase 13, but not early chondrogenic markers, such as Col II or aggrecan, was suppressed in p100-/- mice. An in vivo BrdU tracing assay clearly demonstrated less proliferative activity in chondrocytes in p100-/- mice. These defects were partly rescued when the RelB gene was deleted in p100-/- mice. Taken together, the alternative NF-κB pathway may regulate chondrocyte proliferation and differentiation to maintain endochondral ossification.

    DOI： doi: 10.1002/jcb.29193.

  • Osteocalcin triggers Fas/FasL-mediated necroptosis in adipocytes via activation of p300. Reviewed International journal

    Otani T, Matsuda M, Mizokami A, Kitagawa N, Takeuchi H, Jimi E, Inai T, Hirata M.

    Cell Death Dis. 2018 13: 1194   13   1194   2018.12

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

  • The actin-binding protein PPP1r18 regulates maturation, actin organization, and bone resorption activity of osteoclasts Reviewed

    Takuma Matsubara, Shoichiro Kokabu, Chihiro Nakatomi, Masayuki Kinbara, Toshihiro Maeda, Mitsuhiro Yoshizawa, Hisataka Yasuda, Teruko Takano-Yamamoto, Roland Baron, Eijiro Jimi

    Molecular and Cellular Biology   38 ( 4 )   2018.2

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

    DOI： 10.1128/MCB.00425-17

  • A peptide that blocks the interaction of NF-κB p65 subunit with Smad4 enhances BMP2-induced osteogenesis Reviewed

    2018.1

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

    Bone morphogenetic protein (BMP) potentiates bone formation through the Smad signaling pathway in vitro and in vivo. The transcription factor nuclear factor κB (NF-κB) suppresses BMP-induced osteoblast differentiation. Recently, we identified that the transactivation (TA) 2 domain of p65, a main subunit of NF-κB, interacts with the mad homology (MH) 1 domain of Smad4 to inhibit BMP signaling. Therefore, we further attempted to identify the interacting regions of these two molecules at the amino acid level. We identified a region that we term the Smad4-binding domain (SBD), an amino-terminal region of TA2 that associates with the MH1 domain of Smad4. Cell-permeable SBD peptide blocked the association of p65 with Smad4 and enhanced BMP2-induced osteoblast differentiation and mineralization without affecting the phosphorylation of Smad1/5 or the activation of NF-κB signaling. SBD peptide enhanced the binding of the BMP2-inudced phosphorylated Smad1/5 on the promoter region of inhibitor of DNA binding 1 (Id-1) compared with control peptide. Although SBD peptide did not affect BMP2-induced chondrogenesis during ectopic bone formation, the peptide enhanced BMP2-induced ectopic bone formation in subcortical bone. Thus, the SBD peptide is useful for enabling BMP2-induced bone regeneration without inhibiting NF-κB activity.

    DOI： 10.1002/jcp.26571

  • NOTCH2 Hajdu-Cheney Mutations Escape SCFFBW7-Dependent Proteolysis to Promote Osteoporosis Reviewed

    Hidefumi Fukushima, Kouhei Shimizu, Asami Watahiki, Seira Hoshikawa, Tomoki Kosho, Daiju Oba, Seiji Sakano, Makiko Arakaki, Aya Yamada, Katsuyuki Nagashima, Koji Okabe, Satoshi Fukumoto, Eijiro Jimi, Anna Bigas, Keiichi Nakayama, Keiko Nakayama, Yoko Aoki, Wenyi Wei, Hiroyuki Inuzuka

    Molecular Cell   68 ( 4 )   645 - 658   2017.11

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

    DOI： 10.1016/j.molcel.2017.10.018

  • The transcriptional co-repressor TLE3 regulates myogenic differentiation by repressing the activity of the MyoD transcription factor Reviewed

    Shoichiro Kokabu, Chihiro Nakatomi, Takuma Matsubara, Yusuke Ono, William N. Addison, Jonathan W. Lowery, Mariko Urata, Aaron M. Hudnall, Suzuro Hitomi, Mitsushiro Nakatomi, Tsuyoshi Sato, Kenji Osawa, Tetsuya Yoda, Vicki Rosen, Eijiro Jimi

    Journal of Biological Chemistry   292 ( 31 )   12885 - 12894   2017.1

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

    DOI： 10.1074/jbc.M116.774570

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Books

  • スタンダード生化学・口腔生化学　第4版 Reviewed

    スタンダード生化学・口腔生化学　第4版（ Role： Contributor第３章「酵素・補酵素・ビタミン」第６章「細胞・生命科学」第14章「歯周組織と歯周疾患の生化学」）

    学建書院  2023.3 

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    Language：Japanese   Book type：Textbook, survey, introduction

  • スタンダード生化学・口腔生化学　第３版 Reviewed

    （ Role： Contributor ,  Original_author： スタンダード生化学・口腔生化学　第３版 ,  第３章「酵素・補酵素・ビタミン」第６章「細胞・生命科学」第14章「歯周組織と歯周疾患の生化学」）

    学建書院  2016 

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    Language：Japanese   Book type：Textbook, survey, introduction

  • 「骨ペディア」『骨疾患・骨代謝キーワード事典』

    「骨ペディア」『骨疾患・骨代謝キーワード事典』（ Role： ContributorNF−B」「Srcファミリー」）

    日本骨代謝学会編集  2015 

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    Language：Japanese   Book type：Dictionary, encyclopedia

  • スタンダード生化学・口腔生化学　第２版 Reviewed

    スタンダード生化学・口腔生化学　第２版（ Role： Contributor第３章「酵素・補酵素・ビタミン」第６章「再生医学」）

    学建書院  2009 

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    Language：Japanese   Book type：Textbook, survey, introduction

Presentations

  • 閉経後骨粗しょう症と体重増加の共通分子機構 Invited

    ＠自見　英治郎

    第96回日本生化学会大会  2023.11 

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    Event date： 2024.4

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

    Venue：福岡   Country：Japan  

    超高齢社会において、健康寿命の延伸は重要な課題である。閉経後の女性は、骨密度の低下による骨折リスクや体重の増加による糖尿病や心血管障害のほか、乳がんなど女性特有のがんの発症リスクが上がることが報告されている。エストロゲン欠乏による骨密度の低下と体重増加は各臓器で共通の反応を惹起することが考えられるが、従来これらの疾患は、臓器別に研究や治療が行われてきた。我々は、NF-κB-inducing kinase （NIK）の遺伝的機能欠失型変異によって非古典的経路が抑制されたalymphoplasia（aly/aly）マウスが骨吸収の抑制による軽度の大理石骨病を呈することから、NIKの阻害剤が新たな骨粗鬆症の治療薬になる可能性を考えた。そこで新規NIKの阻害剤Cpd33を卵巣摘出（ovariectomized:OVX）マウスに投与すると、骨量の減少だけでなく、内臓脂肪の増加による体重増加も抑制された。aly/alyマウスにOVXを行った場合でも同様の結果を得た。一方、NF-κBによる骨代謝調節にp65サブユニットの534番セリン残基（S534）のリン酸化が重要なことを見出し、リン酸化を受けないp65変異（S534A）マウスを樹立した。このマウスはNF-κB活性が亢進しており、OVXで誘導される骨量減少と体重増加が著しく亢進した。骨量減少は、破骨細胞による骨吸収の著しい亢進と骨髄細胞からの脂肪細胞への分化亢進に起因し、体重増加は間葉系細胞からの脂肪細胞への分化の亢進に起因すると考えられた。以上の結果より、NF-κBの活性化が閉経後骨粗しょう症と体重増加を制御する標的分子になりうると考えられる。

  • The regulation of NF-κB signaling by p65 serine 534 phosphorylation is involved in both postmenopausal osteoporosis and weight gain

    ＃Fei Huang, ＠Jing Gao,＃ Aonan Li, ＠Akiko　Mizokami,＠Eijiro Jimi

    第65回歯科基礎医学会学術大会  2024.9 

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    Event date： 2024.4

    Language：English  

    Venue：東京   Country：Japan  

  • p130Cas はマウス顎下腺の顆粒性導管細胞分化のための ER-ゴルジネットワークの形成に重要な役割を果たす

    #李 傲男，@高 靖，@藤井 慎介，@清島 保，@自見英治郎

    第64回歯科基礎医学会  2022.9 

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    Event date： 2022.9

    Language：English  

    Venue：徳島   Country：Japan  

  • 閉経による血清RANKL濃度の上昇はNF-kB の非古典的経路を活性化し肥満を引き起こす

    #森 馨代，@溝上 顕子，@佐野 朋美，@兼松 隆，@自見英治郎

    第63回歯科基礎医学会学術大会  2021.10 

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    Event date： 2021.10

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • 新規 NIK 阻害剤の骨吸収阻害薬としての効果の検討

    高倉那奈，@自見英治郎，@松田美穂，#日浦史隆，#森 馨代，　北村知昭

    日本歯科保存学会　2019年度秋季学術大会（第151回）  2019.11 

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    Event date： 2019.11

    Language：Japanese  

    Venue：福岡国際会議場   Country：Japan  

  • 骨吸収の分子機構の解明と歯周病治療への展開 Invited

    @自見　英治郎

    第62回日本歯周病学会学術大会  2020.10 

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    Event date： 2019.10

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

    Venue：西日本総合展示場   Country：Japan  

  • NF-κBとBMPシグナル経路の相互作用を標的とした骨再生の新しいアプローチ Invited

    自見　英治郎

    第60回歯科基礎医学会  2018.9 

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    Event date： 2018.9

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

    Venue：九州大学百年講堂   Country：Japan  

  • 大学院生、基礎研究者そしてPIへ Invited

    自見　英治郎

    先端歯学スクール  2017.8 

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    Event date： 2017.8

    Language：Japanese  

    Venue：東京医科歯科大学   Country：Japan  

  • 骨吸収の分子メカニズム Invited

    自見　英治郎

    第55回日本小児歯科学会大会  2017.6 

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    Event date： 2017.5

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

    Venue：西日本総合展示場、北九州、福岡   Country：Japan  

  • NF-κBシグナルの活性化は卵巣摘出術による骨量減少と体重増加を制御する

    自見英治郎、高靖、溝上顕子、松田美穂、青木和広、片桐岳信、安河内友世

    第66回歯科基礎医学会  2024.11  歯科基礎医学会

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    Event date： 2024.11

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：長崎   Country：Japan  

  • 閉経後骨粗鬆症モデルマウスにおける味覚嗜好性の変容

    川端由子、高井慎吾、岩田周介、實松敬介、兼松隆、自見英治郎、重村憲徳

    第66回歯科基礎医学会学術大会  2024.11  歯科基礎医学会

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    Event date： 2024.11

    Language：Japanese   Presentation type：Poster presentation  

    Venue：長崎   Country：Japan  

  • アルツハイマー病におけるGPRC6A-テストステロンシグナル伝達を介したミクロぐらいの機能調節機構

    社海妍、溝上顕子、佐野朋美、山脇洋輔、自見英治郎、兼松隆

    第66回歯科基礎医学会学術大会  2024.11  歯科基礎医学会

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    Event date： 2024.11

    Language：English   Presentation type：Poster presentation  

    Venue：長崎   Country：Japan  

  • グルタチオン代謝制御を介した4-オクチルイタコン酸の抗腫瘍効果

    佐伯彩華、林慶和、吉本尚平、安河内篤、平田雅人、自見英治郎、安河内友世

    第66回歯科基礎医学会学術大会  2024.11  歯科基礎医学会

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    Event date： 2024.11

    Language：Japanese   Presentation type：Poster presentation  

    Venue：長崎   Country：Japan  

  • イタコン酸を用いたがん進展制御へのアプローチ Invited

    林慶和、佐伯彩華、平田雅人、自見英治郎、安河内友世

    2024.11  歯科基礎医学会

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    Event date： 2024.11

    Language：Japanese   Presentation type：Symposium, workshop panel (nominated)  

    Venue：長崎   Country：Japan  

  • 胎児期栄養環境と成熟後エネルギー代謝以上の因果メカニズムの追求 Invited

    安河内友世、自見英治郎、平田雅人

    第66回歯科基礎医学会学術大会　次世代研究者シンポジウム  2024.11 

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    Event date： 2024.11

    Language：Japanese   Presentation type：Symposium, workshop panel (nominated)  

    Venue：長崎   Country：Japan  

  • Possible Engagement of Distinct Osteoclasts Originated from Dendritic Cells in the Bone Lesion by Squamous Cell Carcinoma

    Miyagawa K, Minohara M, Yamashita S, Takahata S,Shindou S, Suzuki M,, Kawai T, Jimi E , Mikuni-Takagaki Y, Michigami T, Tanaka A, Aikawa T

    ASBMR 2024 Annual Meeting  2024.9  The American Society for Bone and Mineral Research

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    Event date： 2024.9

    Language：English   Presentation type：Poster presentation  

  • Distinct osteoclastogenesis from dendritic cells derived from squamous cell carcinoma of different bone resorption patterns

    Kazuaki Miyagawa, Masato Minohara, Eijiro Jimi, Tomonao Aikawa

    2024.6 

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    Event date： 2024.6 - 2024.7

    Language：Japanese   Presentation type：Poster presentation  

    Country：Japan  

  • NF-κB シグナル伝達の活性化は卵巣摘出による骨量減少と体重増加を調節する

    黄 菲，高 靖，松田 美穂，青木 和広，片桐 岳信， 安河内 友世 ，自見 英治郎

    第42回日本骨代謝学会学術大会  2024.7  日本骨代謝学会

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    Event date： 2024.6 - 2024.7

    Language：English   Presentation type：Oral presentation (general)  

    Venue：沖縄   Country：Japan  

  • 加齢に伴う病態変化の生化学 Invited

    ＠自見　英治郎

    第96回日本生化学会大会  2023.11 

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    Event date： 2024.4

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

    Venue：福岡   Country：Japan  

  • p130Casはエナメル芽細胞分化過程において細胞極性を制御する

    #川原　純平、@吉崎 恵悟、湯田 智美、井上　茜、@宮崎 佳奈子、@田 甜、#韓 涛、@自見　英治郎、@高橋　一郎

    第82回日本矯正歯科学会学術大会  2023.11 

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    Event date： 2024.4

    Language：Japanese  

    Venue：新潟   Country：Japan  

  • 上皮細胞分化と発毛制御における転写因子NF-κB p65サブユニットの役割

    ＃高 田、＠川端 由子、＠清島 保、＠自見 英治郎

    第96回日本生化学会大会  2023.11 

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    Event date： 2024.4

    Language：Japanese  

    Venue：福岡   Country：Japan  

  • The functional implications of deamination in p65, a subunit of NF-κB, in oral squamous cell carcinoma.

    第96回日本生化学会大会  2023.11 

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    Event date： 2024.4

    Language：English  

    Venue：福岡   Country：Japan  

  • 生活環境に起因する 閉経後の骨粗鬆症やエネルギー代謝異常症の進展制御機構

    ＃鞠 超然、＠安河内（川久保）友世、＃高 田、＠小倉 綾乃、＠川端 由子、＠自見 英治郎

    2023.11 

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    Event date： 2024.4

    Language：Japanese  

    Venue：福岡   Country：Japan  

  • NF-κB signaling is involved in both postmenopausal osteoporosis and weight gain

    第96回日本生化学会大会  2023.11 

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    Event date： 2024.4

    Language：Japanese  

    Venue：福岡   Country：Japan  

  • 閉経後の骨・エネルギー代謝異常の進展を制御する環境エンリッチメント

    #鞠 超然、@安河内（川久保）友世、#高 田、@小倉 綾乃、@川端 由子、@自見 英治郎

    第65回歯科基礎医学会学術大会  2023.9 

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    Event date： 2024.4

    Language：Japanese  

    Country：Japan  

  • 転写因子NF-κB p65サブユニットによる上皮細胞分化と発毛制御

    #高 田、@川端 由子、@清島 保、@自見 英治郎

    第65回歯科基礎医学会学術大会  2023.9 

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    Event date： 2024.4

    Language：Japanese  

    Venue：東京   Country：Japan  

  • エナメル芽細胞極性化におけるp130Casの機能解析

    #川原　純平、@吉崎 恵悟、湯田 智美、井上　茜、@宮崎 佳奈子、@田 甜、#韓　涛、@自見　英治郎、@高橋　一郎

    第65回歯科基礎医学会学術大会  2023.9 

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    Event date： 2024.4

    Language：Japanese  

    Country：Japan  

  • Functional analysis of deamination in p65, a subunit of NF-κB, in oral squamous cell carcinoma

    第65回歯科基礎医学会学術大会  2023.9 

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    Event date： 2024.4

    Language：English  

    Country：Japan  

  • The regulatory mechanism of NF-kB signals involved in postmenopausal osteoporosis and weight gain NF-κBシグナルの調節メカニズムは閉経後骨粗鬆症と体重増加に関与する

    第64回歯科基礎医学会  2022.9 

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    Event date： 2023.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：徳島   Country：Japan  

  • 転写因子 NF-κB の新たな活性化制御機構とその機能解析

    #青木 司、@松田 美穂、@自見 英治郎

    第64回歯科基礎医学会  2022.9 

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    Event date： 2022.9

    Language：English   Presentation type：Oral presentation (general)  

    Venue：徳島   Country：Japan  

  • 唾液腺におけるId4の役割と病態への関与

    #木村宗惟、林慶和、#佐伯彩華、安河内篤、@中村誠司、@自見英治郎、@安河内（川久保）友世

    第64回歯科基礎医学会  2022.9 

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    Event date： 2022.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：徳島   Country：Japan  

  • 低分子量Gタンパク質ARL4Cの発現はエナメル上皮腫における腫瘍細胞増殖と破骨細胞形成を促進する

    @藤井 慎介、@自見 英治郎,@清島 保

    第64回歯科基礎医学会  2022.9 

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    Event date： 2022.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：徳島   Country：Japan  

  • 充実環境による閉経後骨粗鬆症・体重増加に対する抑制効果

    #鞠 超然、@川端　由子、#黄 菲、#李 傲男、@自見 英治郎

    第64回歯科基礎医学会  2022.9 

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    Event date： 2022.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：徳島   Country：Japan  

  • 閉経後骨粗鬆症モデルマウスの味覚行動の変化

    ＠川端 由子、#尾池 麻未、@髙井 信吾、@岩田 周介、@實松 敬介、@重村 憲德、@兼松 隆、@自見 英治郎

    2022.9 

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    Event date： 2022.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：徳島   Country：Japan  

  • LC3の阻害は破骨細胞の成熟を抑制し、歯周病モデルの骨破壊を抑制する

    #日浦 史隆、@川端 由子、@溝上 顕子、@自見 英治郎

    第64回歯科基礎医学会  2022.9 

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    Event date： 2022.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • The role of serine 536 phosphorylation of NF-kB p65 in the bone loss and obesity in postmenopausal women

    #Fei Huang, @Jing Gao, @Eijiro Jimi

    2021.10 

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    Event date： 2021.10

    Language：English   Presentation type：Oral presentation (general)  

    Country：Japan  

  • エナメル上皮腫におけるRAF1-MAPK依存性の低分子量Gタンパク質ARL4Cの高発現は腫瘍細胞増殖と破骨細胞形成を促進する

    #小倉 萌，@藤井 慎介，@自見英治郎，@清島 保

    第63回歯科基礎医学会学術大会  2021.10 

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    Event date： 2021.10

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • 唾液腺の形態形成及び機能発現における p130Cas の役割

    #室屋 龍佑，@高 靖，中富 千尋，@藤井 慎介，@清島 保，@自見英治郎

    第61回歯科基礎医学会  2019.10 

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    Event date： 2019.10

    Language：Japanese  

    Country：Japan  

  • p130Cas のエナメル質成熟過程における役割

    井上 茜,　中富 千尋， 中富 満城， 進 正史， 岡部 幸司， 大島 勇人， 松田 美穂， 自見英治郎

    第61回歯科基礎医学会  2019.10 

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    Event date： 2019.10

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：東京歯科大学   Country：Japan  

  • 新規 NIK 阻害剤 Compound33 による破骨細胞分化・機能抑制効果の検討

    高倉 那奈，　松田 美穂，　日浦 史隆，　北村 知昭，　自見英治郎

    第61回歯科基礎医学会  2019.10 

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    Event date： 2019.10

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：東京歯科大学   Country：Japan  

  • オステオカルシンの代謝改善効果における GLP-1 受容体シグナルの役割

    @溝上 顕子　向井 悟　竹内 弘　@自見英治郎　平田 雅人

    第61回歯科基礎医学会  2019.10 

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    Event date： 2019.10

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：東京歯科大学   Country：Japan  

  • 扁平上皮癌細胞の形態変化・移動・浸潤および骨破壊における p130Cas の役割

    柳沼 樹、松原 琢磨、古株彰一郎、中富 千尋、自見英治郎

    第６０回歯科基礎医学会  2018.9 

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    Event date： 2018.9 - 2019.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • オステオカルシンは紫外線誘導性酸化ストレスの抑制作用を有している

    向井 悟、溝上 顕子、高 靖、自見英治郎、平田 雅人

    第６０回歯科基礎医学会  2018.9 

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    Event date： 2018.9

    Language：Japanese  

    Venue：九州大学百年講堂、福岡   Country：Japan  

  • 新規 NIK 阻害剤の RANKL 誘導性破骨細胞分化への影響の検討

    高倉 那奈、松田 美穂、日浦 史隆、北村 知昭、自見英治郎

    第６０回歯科基礎医学会  2018.9 

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    Event date： 2018.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • エナメル質成熟過程における p130Cas の機能解析

    中富 千尋、中富 満城、古株彰一郎、松原 琢磨、大島 勇人、自見英治郎

    第６０回歯科基礎医学会  2018.9 

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    Event date： 2018.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：九州大学百年講堂、福岡   Country：Japan  

  • PRIP による脂肪細胞のインスリンシグナリングの調節

    高 靖、溝上 顕子、竹内 弘、自見英治郎、平田 雅人

    第６０回歯科基礎医学会  2018.9 

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    Event date： 2018.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：九州大学百年講堂、福岡   Country：Japan  

  • p130Cas と結合する分子 Bif-1 は破骨細胞による骨吸収へ影響を与える

    當山 健弥、松原 琢磨、古株彰一郎、中富 千尋、牧 憲司、自見英治郎

    第６０回歯科基礎医学会  2018.9 

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    Event date： 2018.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：九州大学百年講堂、福岡   Country：Japan  

  • 破骨細胞のアクチンリング形成における Kif1c の役割

    小早川美輝、松原 琢磨、古株彰一郎、細川 隆司、自見英治郎

    第６０回歯科基礎医学会  2018.9 

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    Event date： 2018.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：九州大学百年講堂、福岡   Country：Japan  

  • 骨基質タンパク質オステオカルシンと相互作用する分子の探索

    鮫島 潤星、中辻 敬太、加来 謙太、野田純一郎、高 靖、溝上 顕子、松田 美穂、自見英治郎

    第６０回歯科基礎医学会  2018.9 

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    Event date： 2018.9

    Language：Japanese  

    Country：Japan  

  • 唾液腺の発生および機能発現における p130Cas の役割

    室屋 龍佑、高 靖、中富 千尋、藤井 慎介、清島 保、自見英治郎

    第６０回歯科基礎医学会  2018.9 

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    Event date： 2018.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • p130CasはTGFβ刺激による口腔扁平上皮癌の形態変化、細胞移動、および浸潤能の亢進に関与する International conference

    柳沼樹、松原琢磨、古株彰一郎、中富千尋、矢田直美、松尾拡、吉岡泉、自見英治郎

    第78回九州歯科学会総会・学術大会  2018.5 

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    Event date： 2018.5

    Language：Japanese  

    Country：Japan  

  • PPP1r18による破骨細胞分化制御

    松原琢磨、古株彰一郎、中富千尋、自見英治郎

    第78回九州歯科学会総会・学術大会  2018.5 

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    Event date： 2018.5

    Language：English  

    Country：Japan  

  • 新規NIK阻害剤の骨吸収抑制効果の検討

    高倉那奈、自見英治郎、古株彰一郎、松原琢磨、北村知昭

    第78回九州歯科学会総会・学術大会  2018.5 

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    Event date： 2018.5

    Language：Japanese  

    Country：Japan  

  • p130Cas結合タンパク質Bif-1は破骨細胞の骨吸収を制御する

    當山健弥、松原琢磨、古株彰一郎、中富千尋、牧憲司、自見英治郎

    第78回九州歯科学会総会・学術大会  2018.5 

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    Event date： 2018.5

    Language：Japanese  

    Country：Japan  

  • 破骨細胞の成熟過程におけるKif1cの役割

    小早川美輝、松原琢磨、古株彰一郎、細川隆司、自見英治郎

    第78回九州歯科学会総会・学術大会  2018.5 

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    Event date： 2018.5

    Language：Japanese  

    Country：Japan  

  • 破骨細胞のアクチンリング形成および破骨細胞性骨吸収を制御するアクチン結合分子PPP1r18

    松原琢磨、古株彰一郎、中富千尋、自見英治郎

    第59回歯科基礎医学会学術大会  2017.9 

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    Event date： 2017.9 - 2018.9

    Language：Japanese  

    Country：Japan  

  • BMPによる骨形成促進を目的としたSmad4とNF-κB p65の会合領域の検討

    浦田真梨子、松原琢磨、中富千尋、平田-土屋志津、古株彰一郎、張 皿、北村知昭、自見英治郎

    第59回歯科基礎医学会学術大会  2017.9 

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    Event date： 2017.9

    Language：Japanese  

    Country：Japan  

  • 成長板軟骨細胞の増殖におけるNF-κB非古典的経路の役割

    中富千尋、松原琢磨、中富満城、古株彰一郎、自見英治郎

    第59回歯科基礎医学会学術大会  2017.9 

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    Event date： 2017.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • シグナル調節分子PRIPの破骨細胞分化における役割

    松田美穂、自見英治郎、平田雅人

    第59回歯科基礎医学会学術大会  2017.9 

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    Event date： 2017.9

    Language：Japanese  

    Country：Japan  

  • 脂肪組織特異的GPRC6A欠損が全身代謝に与える影響

    溝上顕子、竹内弘、自見英治郎、平田雅人

    第59回歯科基礎医学会学術大会  2017.9 

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    Event date： 2017.9

    Language：Japanese  

    Country：Japan  

  • 悪性黒色腫の顎骨浸潤と転移におけるBMPシグナルの役割

    小川昌洋、古株彰一郎、中富千尋、松原琢磨、渡邉誠之、自見英治郎

    第59回歯科基礎医学会学術大会  2017.9 

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    Event date： 2017.9

    Language：Japanese  

    Country：Japan  

  • 動脈硬化の病態におけるオステオカルシンの役割

    近藤皓彦、川久保-安河内友世、溝上顕子、自見英治郎、平田雅人

    第59回歯科基礎医学会学術大会  2017.9 

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    Event date： 2017.9

    Language：Japanese  

    Country：Japan  

  • TLE3による骨格筋組織幹細胞、サテライト細胞の増殖・分化制御機構

    古株彰一郎、中富千尋、松原琢磨、自見英治郎

    第59回歯科基礎医学会学術大会  2017.9 

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    Event date： 2017.9

    Language：Japanese  

    Country：Japan  

  • 閉経後骨粗鬆症モデルマウスの味覚行動の変化(The behavioral taste responses of postmenopausal osteoporosis in mice)

    川端 由子, 尾池 麻未, 高井 信吾, 岩田 周介, 實松 敬介, 重村 憲徳, 兼松 隆, 自見 英治郎

    Journal of Oral Biosciences Supplement  2022.9  (一社)歯科基礎医学会

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    Language：Japanese  

  • 閉経後骨粗鬆症モデルマウスの味覚変調とその分子機構の解析

    川端 由子, 高井 信吾, 岩田 周介, 實松 敬介, 兼松 隆, 自見 英治郎, 重村 憲徳

    Journal of Oral Biosciences Supplement  2023.9  (一社)歯科基礎医学会

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    Language：Japanese  

  • 閉経後骨粗鬆症モデルマウスにおける金属味感受性の変化(Modification of metallic taste in postmenopausal osteoporosis model mice)

    Kawabata Yuko, Takai Shingo, Iwata Shusuke, Sanematsu Keisuke, Kawabata Fuminori, Kanematsu Takashi, Jimi Eijiro, Shigemura Noriatsu

    The Journal of Physiological Sciences  2024.5  (一社)日本生理学会

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    Language：English  

  • 転写因子NF-κBの新たな活性化制御機構とその機能解析(Analysis of novel regulatory mechanism of nuclear factor-κB)

    青木 司, 松田 美穂, 自見 英治郎

    Journal of Oral Biosciences Supplement  2022.9  (一社)歯科基礎医学会

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    Language：Japanese  

  • 転写因子NF-k B p65サブユニットによる上皮細胞分化と発毛制御

    高 田, 川端 由子, 清島 保, 自見 英治郎

    Journal of Oral Biosciences Supplement  2023.9  (一社)歯科基礎医学会

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    Language：Japanese  

  • 脂肪酸代謝におけるid4の役割

    朱 栄忠, 林 慶和, 木村 宗惟, 矢野 恵奈, 畠山 雄次, 平田 雅人, 自見 英治郎, 羅 翊禎, 安河内 友世[川久保]

    日本生化学会大会プログラム・講演要旨集  2023.10  (公社)日本生化学会

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    Language：English  

  • 脂肪組織と肝臓のエネルギー代謝におけるId4の役割(The role of Id4 on energy metabolism in adipose tissue and liver)

    Zhu Rongzhong, Hayashi Yoshikazu, Kimura Soi, Hatakeyama Yuji, Hirata Masato, Jimi Eijiro, Kawakubo-Yasukochi Tomoyo

    Journal of Oral Biosciences Supplement  2023.9  (一社)歯科基礎医学会

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  • 糖類センサーとしてのGPRC5Cの機能分析(The functional analysis of GPRC5C as a saccharide sensor)

    Takai Shingo, Kawabata Yuko, Sanematsu Keisuke, Iwata Syusuke, Kawabata Fuminori, Kanematsu Takashi, Jimi Eijiro, Shigemura Noriatsu

    The Journal of Physiological Sciences  2024.5  (一社)日本生理学会

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  • 性ホルモンのテストステロンがミクログリアにおけるNF-κB炎症経路を抑制する(Sex hormone testosterone inhibits NF-K B inflammatory pathway in microglia)

    Zheng Haolin, Mizokami Akiko, Kanematsu Takashi, Sano Tomomi, Yamawaki Yosuke, Jimi Eijiro

    Journal of Oral Biosciences Supplement  2023.9  (一社)歯科基礎医学会

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    Language：English  

  • 唾液腺におけるId4の役割と病態への関与(The role of Id4 in the salivary gland and its involvement in pathology)

    木村 宗惟, 林 慶和, 佐伯 彩華, 安河内 篤, 中村 誠司, 自見 英治郎, 安河内 友世[川久保], 矢野 恵奈, 森山 雅文

    Journal of Oral Biosciences Supplement  2022.9  (一社)歯科基礎医学会

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    Language：Japanese  

  • 口腔扁平上皮癌におけるNF-κBのサブユニットであるp65の脱アミノ化の機能的意義(The functional implications of deamination in p65, a subunit of NF-κB, in oral squamous cell carcinoma)

    Tu Yiran, Ogura Ayano, Jimi Eijiro

    日本生化学会大会プログラム・講演要旨集  2023.10  (公社)日本生化学会

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    Language：English  

  • 加齢に伴う病態変化の生化学　閉経後骨粗しょう症と体重増加の共通分子機構

    自見 英治郎

    日本生化学会大会プログラム・講演要旨集  2023.10  (公社)日本生化学会

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    Language：Japanese  

  • 充実環境による閉経後骨粗鬆症・体重増加に対する抑制効果(Inhibitory effects on postmenopausal osteoporosis and weight gain in enriched environment)

    鞠 超然, 川端 由子, 李 傲男, 黄 菲, 片桐 岳信, 自見 英治郎

    Journal of Oral Biosciences Supplement  2022.9  (一社)歯科基礎医学会

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    Language：Japanese  

  • 低分子量Gタンパク質ARL4Cの発現はエナメル上皮腫における腫瘍細胞増殖と破骨細胞形成を促進する(RAF1-MEK/ERK pathway-dependent ARL4C expression promotes ameloblastoma cell proliferation and osteoclast formation)

    藤井 慎介, 自見 英治郎, 清島 保

    Journal of Oral Biosciences Supplement  2022.9  (一社)歯科基礎医学会

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    Language：Japanese  

  • ミクログリアのオートファジー誘導におけるGPRC6A-テストステロンシグナルの役割

    杜 海妍, 溝上 顕子, 兼松 隆, 佐野 朋美, 山脇 洋輔, 自見 英治郎

    日本生化学会大会プログラム・講演要旨集  2023.10  (公社)日本生化学会

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    Language：English  

  • ミクログリアにおけるmiRNA発現の性差(Differences in microRNA expression patterns contribute to sexually differential characteristics of microglia)

    溝上 顕子, 佐野 朋美, 山脇 洋輔, 自見 英治郎, 兼松 隆

    Journal of Oral Biosciences Supplement  2022.9  (一社)歯科基礎医学会

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    Language：Japanese  

  • テストステロンはmiRNA3535を介した脂肪酸合成制御にようりミクログリアにおける炎症反応を抑制する

    鄭 昊林, 溝上 顕子, 兼松 隆, 佐野 朋美, 山脇 洋輔, 自見 英治郎

    日本生化学会大会プログラム・講演要旨集  2023.10  (公社)日本生化学会

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    Language：English  

  • エナメル芽細胞極性化におけるp130Casの機能解析

    川原 純平, 吉崎 恵悟, 湯田 智美, 井上 茜, 宮崎 佳奈子, 田 甜, 自見 英治郎, 高橋 一郎

    Journal of Oral Biosciences Supplement  2023.9  (一社)歯科基礎医学会

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    Language：Japanese  

  • エナメル上皮腫における低分子量Gタンパク質ARL4Cの発現は腫瘍細胞増殖と破骨細胞形成を促進する

    藤井 慎介, 自見 英治郎, 清島 保

    日本病理学会会誌  2022.3  (一社)日本病理学会

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    Language：Japanese  

  • イタコン酸によるがん細胞抗酸化システムの制御

    佐伯 彩華, 林 慶和, 吉本 尚平, 畠山 雄次, 平田 雅人, 自見 英治郎, 安河内 友世[川久保]

    Journal of Oral Biosciences Supplement  2023.9  (一社)歯科基礎医学会

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    Language：Japanese  

  • アルツハイマー病の性差の分子基盤におけるミクログリアの役割解明(Elucidating the role of microglia in the molecular basis of sex differences in Alzheimer's disease)

    Du Haiyan, Mizokami Akiko, Kanematsu Takashi, Sano Tomomi, Yamawaki Yosuke, Jimi Eijiro

    Journal of Oral Biosciences Supplement  2023.9  (一社)歯科基礎医学会

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    Language：English  

  • p65セリン534リン酸化によるNF-κBシグナル伝達の制御は閉経後骨粗鬆症と体重増加に関与する(The regulation of NF-K B signaling by p65 serine 534 phosphorylation is involved in both postmenopausal osteoporosis and weight gain)

    Huang Fei, Gao Jing, Li Aonan, Mizokami Akiko, Jimi Eijiro

    Journal of Oral Biosciences Supplement  2023.9  (一社)歯科基礎医学会

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    Language：English  

  • p130casはマウス顎下腺の顆粒性導管細胞分化のためのER-ゴルジネットワークの形成に重要な役割を果たす(p130cas plays a crucial role in ER-Golgi network formation for cell differentiation of granular convoluted tubules in mouse submandibular glands)

    李 傲男, 高 靖, 藤井 慎介, 清島 保, 自見 英治郎

    Journal of Oral Biosciences Supplement  2022.9  (一社)歯科基礎医学会

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    Language：English  

  • NF-κB非古典経路の阻害は歯周組織の炎症と骨吸収を抑制する

    青木 司, 自見 英治郎, 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  2023.10  (NPO)日本歯科保存学会

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    Language：Japanese  

  • NF-κBシグナル経路は閉経後骨粗鬆症と体重増加の両方に関与する

    黄 菲, 高 靖, 李 傲男, 溝上 顕子, 自見 英治郎

    日本生化学会大会プログラム・講演要旨集  2023.10  (公社)日本生化学会

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    Language：English  

  • NF-ΚBシグナルの調節メカニズムは閉経後骨粗鬆症と体重増加に関与する(The regulatory mechanism of NF-ΚB signals involved in postmenopausal osteoporosis and weight gain)

    黄 菲, 高 靖, 李 傲男, 溝上 顕子, 自見 英治郎

    Journal of Oral Biosciences Supplement  2022.9  (一社)歯科基礎医学会

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    Language：English  

  • LC3の阻害は破骨細胞の成熟を抑制し、歯周病モデルの骨破壊を抑制する(Inhibition of LC3 suppresses osteoclast maturation and bone destruction in periodontal disease models)

    日浦 史隆, 川端 由子, 溝上 顕子, 自見 英治郎

    Journal of Oral Biosciences Supplement  2022.9  (一社)歯科基礎医学会

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    Language：Japanese  

  • GPRC5ファミリーによる糖受容機構の探索

    高井 信吾, 川端 由子, 實松 敬介, 岩田 周介, 兼松 隆, 自見 英治郎, 重村 憲徳

    Journal of Oral Biosciences Supplement  2023.9  (一社)歯科基礎医学会

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    Language：Japanese  

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MISC

  • The unique function of p130Cas in regulating the bone metabolism. Reviewed

    Jimi E, Honda H, Nakamura I.

    Pharmacol Ther.   2021.10

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

    DOI： 10.1016/j.pharmthera.2021.1

  • Critical roles of NF-κB signaling molecules in bone metabolism revealed by genetic mutation in osteopetrosis. Reviewed

    2022.7

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 臨床に向けた最近の研究動向から 最新の骨代謝研究について―第２回　新たな骨粗鬆症治療薬の開発

    自見　英治郎

    日本歯科評論   2020.11

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 臨床に向けた最近の研究動向から 最新の骨代謝研究について―第３回　口腔癌による顎骨浸潤の治療標的分子 Reviewed

    自見　英治郎

    日本歯科評論   2020.11

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 臨床に向けた最近の研究動向から 最新の骨代謝研究について―第１回　BMP2を用いた新たな骨再生の試み

    自見　英治郎

    日本歯科評論 10月号   2020.10

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 新たな骨粗しょう症治療薬開発への期待

    自見　英治郎

    2020.8

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • NF-κB signaling regulates physiological and pathological chondrogenesis.

    2019.12

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

    The nuclear factor-κB (NF-κB) is a transcription factor that regulates the expression of genes that control cell proliferation and apoptosis, as well as genes that respond to inflammation and immune responses. There are two means of NF-κB activation: the classical pathway, which involves the degradation of the inhibitor of κBα (IκBα), and the alternative pathway, which involves the NF-κB-inducing kinase (NIK, also known as MAP3K14). The mouse growth plate consists of the resting zone, proliferative zone, prehypertrophic zone, and hypertrophic zone. The p65 (RelA), which plays a central role in the classical pathway, is expressed throughout the cartilage layer, from the resting zone to the hypertrophic zone. Inhibiting the classical NF-κB signaling pathway blocks growth hormone (GH) or insulin-like growth factor (IGF-1) signaling, suppresses cell proliferation, and suppresses bone morphogenetic protein 2 (BMP2) expression, thereby promoting apoptosis. Since the production of autoantibodies and inflammatory cytokines, such as tumor necrosis factor-α (TNFα), interleukin (IL)-1β, IL-6, and IL-17, are regulated by the classical pathways and are increased in rheumatoid arthritis (RA), NF-κB inhibitors are used to suppress inflammation and joint destruction in RA models. In osteoarthritis (OA) models, the strength of NF-κB-activation is found to regulate the facilitation or suppression of OA. On the other hand, RelB is involved in the alternative pathway, and is expressed in the periarticular zone during the embryonic period of development. The alternative pathway is involved in the generation of chondrocytes in the proliferative zone during physiological conditions, and in the development of RA and OA during pathological conditions. Thus, NF-κB is an important molecule that controls normal development and the pathological destruction of cartilage.

    DOI： doi: 10.3390/ijms20246275.

  • The Role of NF-κB in physiological bone development and Inflammatory bone diseases: Is NF-κB Inhibition "Killing two birds with one stone"?

    2019.12

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

    Nuclear factor-κB (NF-κB) is a transcription factor that regulates the expression of various genes involved in inflammation and the immune response. The activation of NF-κB occurs via two pathways: inflammatory cytokines, such as TNF-α and IL-1β, activate the "classical pathway", and cytokines involved in lymph node formation, such as CD40L, activate the "alternative pathway". NF-κB1 (p50) and NF-κB2 (p52) double-knockout mice exhibited severe osteopetrosis due to the total lack of osteoclasts, suggesting that NF-κB activation is required for osteoclast differentiation. These results indicate that NF-κB may be a therapeutic target for inflammatory bone diseases, such as rheumatoid arthritis and periodontal disease. On the other hand, mice that express the dominant negative form of IκB kinase (IKK)-β specifically in osteoblasts exhibited increased bone mass, but there was no change in osteoclast numbers. Therefore, inhibition of NF-κB is thought to promote bone formation. Taken together, the inhibition of NF-κB leads to "killing two birds with one stone": it suppresses bone resorption and promotes bone formation. This review describes the role of NF-κB in physiological bone metabolism, pathologic bone destruction, and bone regeneration.

    DOI： doi: 10.3390/cells8121636.

  • 破骨細胞

    自見　英治郎

    副甲状腺・骨代謝疾患診療マニュアル   2019.6

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • Vitamin status and mineralized tissue formation

    Eijiro Jimi

    Current Oral Health Reports   2019.2

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 骨リモデリングにおける破骨細胞の役割

    自見　英治郎

    2017.12

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

    骨リモデリングは、破骨細胞による骨吸収と骨芽細胞による骨形成サイクルから成り、骨量とカルシウムの恒常性の維持に重要である。骨吸収と骨形成は密接な関係を保つが、これら２つのバランスが崩れると骨量の増加や減少が生じる。破骨細胞は生理的、または病的骨吸収に関わる多核巨細胞であり、破骨細胞による骨吸収はさまざまなサイトカイン、カルシウムシグナルや転写因子によって制御されている。近年では遺伝子欠損マウスの結果から破骨細胞による骨吸収を制御する新たな分子の重要性が証明されている。本稿では、骨リモデリングを制御する破骨細胞の骨吸収に関する分子機構について最近の知見を概説する。

  • 骨吸収の分子メカニズム

    自見　英治郎

    小児歯科臨床   2017.11

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

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Professional Memberships

  • 日本骨代謝学会

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  • 歯科基礎医学会

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  • 歯科基礎医学会

  • 日本骨代謝学会

  • 分子生物学会

  • 日本生化学会

  • 日本歯科医学教育学会

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Committee Memberships

  • Organizer   Domestic

    2022.12 - 2023.11   

  • Executive   Domestic

    2022.1 - 2024.12   

  • 歯科基礎医学会   常任理事   Domestic

    2022.1 - 2024.12   

  • Executive   Domestic

    2020.5 - 2022.6   

  • Executive   Domestic

    2018.5 - 2019.6   

  • Councilor   Domestic

    2017.10 - 2022.6   

  • 日本骨代謝学会   教育委員会   Domestic

    2017.10 - 2022.6   

  • 九州大学   OBT研究センター長  

    2017.4 - 2028.3   

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    Committee type：Other

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  • 日本骨代謝学会   教育委員会委員   Domestic

    2014.4 - 2020.4   

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Academic Activities

  • シンポジウム企画

    Role(s)： Planning, management, etc.

    歯科基礎医学会  2024.11

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    Type：Academic society, research group, etc. 

    Number of participants：80

  • Screening of academic papers

    Role(s)： Peer review

    2024

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    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：29

  • シンポジウム企画

    第96回日本生化学会大会  （ 福岡 ） 2023.10 - 2023.11

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    Type：Competition, symposium, etc. 

  • 幹事

    第96回日本生化学会大会  （ 福岡 ） 2023.4 - 2024.3

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    Type：Competition, symposium, etc. 

  • 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：8

  • シンポジウムオーガナイザー

    歯科基礎医学会  （ 徳島 ） 2022.9

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    Type：Competition, symposium, etc. 

  • Journal of Cellular Physiology International contribution

    Role(s)： Peer review

    2022.4

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    Type：Academic society, research group, etc. 

  • 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：28

  • シンポジウムオーガナイザー

    日本骨代謝学会  （ WEB開催 ） 2021.10 - 2023.10

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    Type：Competition, symposium, etc. 

    Number of participants：300

  • 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：43

  • 国際科学研究費専門委員

    Role(s)： Review, evaluation

    日本学術振興会  2020.6 - 2020.10

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    Type：Scientific advice/Review 

  • 歯科医師国家試験 試験委員

    厚生労働省  2020.4 - 2022.3

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  • 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：37

  • Cells International contribution

    2019.7 - 2021.7

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    Type：Academic society, research group, etc. 

  • 国際科学研究費専門委員

    Role(s)： Review, evaluation

    日本学術振興会  2019.6 - 2019.11

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    Type：Scientific advice/Review 

  • H31基盤研究（Ｓ）研究進捗評価

    Role(s)： Review, evaluation

    日本学術振興会  2019.4 - 2019.6

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    Type：Scientific advice/Review 

  • 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：33

    Proceedings of domestic conference Number of peer-reviewed papers：1

  • 科研研究費審査員

    Role(s)： Review, evaluation

    日本学術振興会  2018.10 - 2019.3

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    Type：Scientific advice/Review 

  • 準備委員長

    第60回歯科基礎医学会学術大会  （ 九州大学医学部百年講堂 ） 2018.9

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    Type：Competition, symposium, etc. 

    Number of participants：1,000

  • Journal of Bone and Mineral Metabolism International contribution

    Role(s)： Peer review

    2018.4 - 2018.6

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    Type：Academic society, research group, 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：20

  • 科学研究費審査員

    Role(s)： Review, evaluation

    日本学術振興会  2017.10 - 2018.3

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    Type：Scientific advice/Review 

  • 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：19

  • Journal of Bone and Mineral Metabolism International contribution

    2010.4 - 2021.3

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    Type：Academic society, research group, etc. 

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Research Projects

  • NF-κBによる骨代謝調節の分子基盤の解明と新たな治療戦略への展開

    Grant number：24KK0167  2024.9 - 2028.3

    科学研究費助成事業  国際共同研究加速基金(海外連携研究)

    自見 英治郎

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    Grant type：Scientific research funding

    CiNii Research

  • Elucidation of the mechanism of resistance acquisition to super-enhancer-targeted anticancer therapies and novel strategies based on this mechanism

    Grant number：24K22193  2024.6 - 2027.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Challenging Research (Exploratory)

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    Grant type：Scientific research funding

    CiNii Research

  • Elucidation of the mechanism of jaw bone destruction caused by oral tumor-stromal interaction.

    Grant number：24K02615  2024.4 - 2028.3

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

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    Grant type：Scientific research funding

    CiNii Research

  • 女性ホルモン欠乏によるNF-κB活性化機構と骨・エネルギー代謝制御の解明

    Grant number：24K02612  2024 - 2026

    日本学術振興会  科学研究費助成事業  基盤研究(B)

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 新規骨補填剤の機能解析

    2023.4 - 2025.4

    共同研究

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    Authorship：Collaborating Investigator(s) (not designated on Grant-in-Aid)  Grant type：Other funds from industry-academia collaboration

  • 超早期癌発見戦略に向けた変異細胞-隣接正常細胞-間質細胞における不安定性出現解明

    Grant number：23H03102  2023 - 2026

    日本学術振興会  科学研究費助成事業  基盤研究(B)

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

  • 膜貫通型受容体ALK2の細胞内二量体の形成を制御する新規分子の探索

    Grant number：23K18343  2023 - 2024

    日本学術振興会  科学研究費助成事業  挑戦的研究（萌芽）

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

  • 上皮系細胞による新たな骨代謝調節機構の解明

    Grant number：23K18363  2023 - 2024

    日本学術振興会  科学研究費助成事業  挑戦的研究（萌芽）

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • Analysis of common molecular mechanisms associated with epithelium differentiation and hair growth

    Grant number：21K19578  2021.7 - 2023.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Challenging Research (Exploratory)

    Katagiri Takenobu

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    Grant type：Scientific research funding

    We established a mouse line of epithelium-specific conditional knockout of Smad4 by crossing Smad4 floxed mice with Keratin 14-Cre mice. These mice showed an abnormal tooth development phenotype, which is regulated by the epithelial-mesenchymal interaction. In RNA-seq analysis using control and Smad4 cKO mice, the expression levels of a gene involved in hair growth were changed in Smad4 cKO mice.

    CiNii Research

  • 硬組織の形成と代謝に関する分子的制御機構の解明と応用に関する研究

    2021.2 - 2024.3

    共同研究

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    Authorship：Principal investigator  Grant type：Other funds from industry-academia collaboration

  • 閉経後の骨粗鬆症と体重増加を制御する本質的共通分子機構の解明と治療戦略への展開

    Grant number：21H03108  2021 - 2023

    日本学術振興会  科学研究費助成事業  基盤研究(B)

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 閉経後の骨粗鬆症と体重増加を制御する本質的共通分子機構の解明と治療戦略への展開

    Grant number：21H03108  2021 - 2023

    日本学術振興会  科学研究費助成事業  基盤研究(B)

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • タンパク質脱アミド化の新たな制御機構の解明と口腔がん細胞を用いた機能解析

    Grant number：21K19609  2021 - 2022

    日本学術振興会  科学研究費助成事業  挑戦的研究（萌芽）

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 器官再生を目指した細胞リソースとしての人為的上皮細胞誘導技術の開発

    Grant number：20K20612  2020.7 - 2024.3

    科学研究費助成事業  挑戦的研究(開拓)

    福本 敏, 吉崎 恵悟, 犬塚 博之, 自見 英治郎, 阪井 丘芳, 山田 亜矢

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    Grant type：Scientific research funding

    これまで再生技術は、胎児や成人組織に存在するわずかな幹細胞の利用、多能性細胞であるES細胞やiPS細胞の応用によるもであった。しかしながら、倫理的な側面や高コストであるなど問題も多く。また器官形成や臓器形成に関して、複雑な培養技術を用いる必要があり、さらには機能的な大型器官や臓器を作成する為に血管や神経構築が必要であることなど、具体的な課題は明確であるが、現時点で画期的な解決方法が存在しない。
    そこで本研究では、器官再生に必要な上皮系細胞の人為的誘導法を開発し、低コストで簡便な器官再生技術開発を行う。

    CiNii Research

  • 感情と免疫学的健康の新しいセンサーとしての骨の働き International coauthorship

    2020.4 - 2023.3

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    Authorship：Principal investigator 

    精神状態と骨代謝疾患の発症や進行との関連が報告されているが、これまで客観的に細胞・分子レベルで解析した研究は殆どない。D’Acquisto教授は、充実環境と社会的孤立という異なる環境下で飼育したマウスに細菌感染実験を行ったところ、充実環境で飼育したマウスは、免疫応答が向上し、社会的孤立では逆の効果を示すことを報告した。本国際共同研究では、充実環境と社会的孤立に代表される生活環境の違いによる精神状態の変化が骨代謝疾患の発症や進行に関与すること、両者の関連にNF-κBが関与すること、さらに精神状態を考慮に入れた新しい骨代謝疾患の予防法、治療法の選択や予後の予測に情報を提供することを目指す。

  • Analysis of molecular mechanisms of bone formation and heterotopic calcification

    Grant number：20H03808  2020.4 - 2023.3

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

    Katagiri Takenobu

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    Grant type：Scientific research funding

    BMP and Wnt signaling is important for bone and tooth development. We found that Wnt7b is essential for BMP-induced bone formation. We developed blocking antibodies against BMP receptors. We identified Wnt7b as the bone-inducing factor produced by hypertrophic chondrocytes during endochondral ossification. Furthermore, we found chemical compounds that stimulate Wnt7b activity in vitro. We developed a mouse model of trauma-induced mineralization of muscle tissue and found that the hard tissue formed is an artificial calcification, but not bone formation.

    CiNii Research

  • Elucidation of high-calorie taste mechanism that connects food intake disorder and addiction

    Grant number：20H03855  2020.4 - 2023.3

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

    Yasumatsu Keiko

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    Grant type：Scientific research funding

    Why do humans eat unnecessary high-calorie foods? In this study, we aimed to explore the regulation of fat taste sensitivity, and investigated which receptors are involved in preference for fatty acids with focus on the hedonic aspects.
    When the correlation coefficient was calculated between the detection threshold for human oleic acid and all questionnaire items, there was a significant correlation between averaged dietary fat intake over the last three days and no correlation with BMI. Multiple SNPs were detected in a whole exome sequencing of GPR120.It was revealed that fatty acids applied to the tongue are transmitted to the brain as sweet and umami taste by mouse glossopharyngeal nerve, and that CD36 and GPR40 play a role as their receptors.

    CiNii Research

  • Development of Hard Tissue Regeneration Therapy via Modulation of Estrogen Signaling by MTI-II

    Grant number：20K09956  2020.4 - 2023.3

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

    Tsuchiya Shizu

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    Grant type：Scientific research funding

    Estrogen contributes to the suppression of the onset and progression of various diseases. Since estrogen receptor (ERa, ERb) expression was found in dental pulp cells established from extracted teeth of patients who consented to the study, we compared the hard tissue-forming ability of pulp cells by sex and found no significant difference in ALP activity. However, both cell types showed increased gene expression of Id1, a BMP response gene. The expression of Caspase 3 and 8 genes was also suppressed. Furthermore, knockdown of Id1 gene expression resulted in suppression of cell proliferation and an increase in apoptosis-positive cells. This suggests that Id1 may be involved in apoptosis of human dental pulp cells.

    CiNii Research

  • Elucidating the mechanisms to induce ameloblastoma and its trial for the clinical setting

    Grant number：20K09906  2020.4 - 2023.3

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

    Fujii Shinsuke

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    Grant type：Scientific research funding

    Ameloblastoma is an odontogenic neoplasm characterized by slow intraosseous growth with progressive jaw resorption. Recent reports revealed that ameloblastoma harbors an oncogenic BRAF V600E mutation with MAPK pathway activation. However, the precise mechanism by which MAPK pathway induces ameloblastoma is unclear. In immunohistochemical analyses of tissue specimens obtained from ameloblastoma patients, ARL4C was frequently expressed with both BRAF V600E and RAF1. ARL4C-depleted tumour cells exhibited decreased proliferation and migration capabilities. Finally, when ameloblastoma cells were co-cultured with mouse bone marrow cells and primary osteoblasts, ameloblastoma cells induced osteoclast formation. ARL4C elevation in ameloblastoma further promoted its formation capabilities. These results suggest that the RAF1-MEK/ERK-ARL4C axis, which may function in cooperation with the BRAF V600E-MEK/ERK pathway, promotes ameloblastoma development.

    CiNii Research

  • The elucidation of the role of NIK in estrogen deficiency-induced diseases

    Grant number：20K09890  2020.4 - 2023.3

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

    Mukai Satoru

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    Grant type：Scientific research funding

    Menopausal women are susceptible to visceral obesity. Circulating levels of receptor activator of nuclear factor kappa B (NF-κB) ligand (RANKL) are elevated in an animal model of menopause. RANKL activates a pivotal mediator of inflammatory responses, the NF-κB pathway. Here, we investigated whether RANKL-induced non-canonical NF-κB pathway activation induces inflammation and lipid accumulation in adipose tissues. We therefore analyzed aly/aly mice, in which the non-canonical NF-κB pathway is not activated. A postmenopausal obesity model was generated by ovariectomy and subsequent high-fat and high-sucrose diet feeding. In aly/aly mice, serum RANKL levels were elevated, and hepatic lipid accumulation and adipocyte hypertrophy were suppressed. Furthermore, aly/aly mice showed protection from glucose intolerance and insulin resistance. These findings indicate that non-canonical NF-κB pathway activation via serum RANKL elevation contributes to postmenopausal obesity.

    CiNii Research

  • 感情と免疫学的健康の新しいセンサーとしての骨の働き

    Grant number：20KK0213  2020 - 2023

    日本学術振興会  科学研究費助成事業  国際共同研究強化(B)

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • Elucidation of correlation between therapeutic effect and gene polymorphism by stellate ganglion block

    Grant number：19K10349  2019.4 - 2024.3

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

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    Grant type：Scientific research funding

    CiNii Research

  • Src-Casを中心とした骨吸収活性調節におけるKifファミリー分子の役割解明

    Grant number：18K09509  2018 - 2020

    日本学術振興会  科学研究費助成事業  基盤研究(C)

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

  • 肥満を引き起こす新たな組織・分子基盤の解明

    Grant number：18H02967  2018 - 2020

    日本学術振興会  科学研究費助成事業  基盤研究(B)

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 病的な骨形成調節機構の解明とその応用

    Grant number：17H04317  2017 - 2019

    日本学術振興会  科学研究費助成事業  基盤研究(B)

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

  • 悪性黒色腫の上皮-間葉移行におけるBMPの役割と新規浸潤・転移モデルの確立

    Grant number：17K11622  2017 - 2019

    日本学術振興会  科学研究費助成事業  基盤研究(C)

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

  • NSAIDsリポジショニングによるNF-κB阻害を介した歯髄炎治療法の開発

    Grant number：17K11706  2017 - 2019

    日本学術振興会  科学研究費助成事業  基盤研究(C)

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

  • 口腔扁平上皮癌上皮間葉移行におけるp130 Casの役割と治療標的としての可能性

    Grant number：17K11884  2017 - 2019

    日本学術振興会  科学研究費助成事業  基盤研究(C)

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

  • 副作用の少ない小児ステロイド性顎骨骨粗鬆症治療における骨吸収阻害薬の開発

    Grant number：17K11968  2017 - 2019

    日本学術振興会  科学研究費助成事業  基盤研究(C)

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

  • 形づくりから分化を制御するp130Casの器官形成における共通性（コモナリティ）

    Grant number：17K19773  2017 - 2018

    科学研究費助成事業  挑戦的萌芽研究

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 埼玉医科大学FOP診療・研究プロジェクト

    2014.6 - 2018.6

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    Authorship：Coinvestigator(s) 

  • SPOCK-1生体タンパクを応用した安全性に優れた革新的歯周病予防薬の開発

    Grant number：19K22721 

    西村 英紀, 自見 英治郎, 佐野 朋美

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    Grant type：Scientific research funding

    歯周炎による組織破壊は感染の結果生体で惹起される炎症によってもたらされる。つまり、予防の観点からは、感染源の制御に加え、宿主の破壊因子の制御が効果的である。spock-1は複数のドメインから構成され、cysteine protease阻害ドメインに加え、複数の酵素を阻害する。申請者らは歯肉増殖症モデルとしてSPOCK-1 transgenic (TG) マウスを樹立した。そこで、逆にspock-1は歯周炎等の炎症性組織破壊に対して抑制的に作用するとの仮説を設けた。本申請では、spock-1TGマウスにおいて実験的歯周炎や硬組織の吸収が抑制され、軟組織の治癒が促進されるか否かを検証する。

    CiNii Research

▼display all

Award for Educational Activities

  • Best Teacher賞

    2012   九州歯科大学  

    Award-winner：自見　英治郎

    学生および同僚による評価で１位となった

Class subject

  • 口腔生化学４

    2024.12 - 2025.2   Winter quarter

  • 口腔生化学３

    2024.10 - 2024.12   Fall quarter

  • 口腔生化学２

    2024.6 - 2024.8   Summer quarter

  • 口腔生化学１

    2024.4 - 2024.6   Spring quarter

  • 口腔細胞工学（高年次）D

    2023.12 - 2024.2   Winter quarter

  • 口腔生化学４

    2023.12 - 2024.2   Winter quarter

  • 口腔細胞工学（低年次）D

    2023.12 - 2024.2   Winter quarter

  • 口腔細胞工学（コア）D

    2023.12 - 2024.2   Winter quarter

  • 口腔細胞工学（高年次）C

    2023.10 - 2023.12   Fall quarter

  • 口腔生化学３

    2023.10 - 2023.12   Fall quarter

  • 口腔細胞工学（低年次）C

    2023.10 - 2023.12   Fall quarter

  • 口腔細胞工学（コア）C

    2023.10 - 2023.12   Fall quarter

  • 口腔細胞工学（高年次）B

    2023.6 - 2023.8   Summer quarter

  • 口腔生化学２

    2023.6 - 2023.8   Summer quarter

  • 口腔細胞工学（低年次）B

    2023.6 - 2023.8   Summer quarter

  • 口腔細胞工学（コア）B

    2023.6 - 2023.8   Summer quarter

  • 口腔細胞工学（高年次）A

    2023.4 - 2023.6   Spring quarter

  • 口腔生化学１

    2023.4 - 2023.6   Spring quarter

  • 口腔細胞工学（低年次）A

    2023.4 - 2023.6   Spring quarter

  • 口腔細胞工学（コア）A

    2023.4 - 2023.6   Spring quarter

  • 口腔細胞工学（高年次）D

    2022.12 - 2023.2   Winter quarter

  • 口腔脳機能病態学（低年次）　D

    2022.12 - 2023.2   Winter quarter

  • 口腔脳機能病態学（コア）　D

    2022.12 - 2023.2   Winter quarter

  • 口腔細胞工学（コア）　D

    2022.12 - 2023.2   Winter quarter

  • 口腔細胞工学（低年次）　D

    2022.12 - 2023.2   Winter quarter

  • Oral,Brain and Total Health Science (Core)　D

    2022.12 - 2023.2   Winter quarter

  • Molecular and Cellular Biochemistry (Lower-grade) D

    2022.12 - 2023.2   Winter quarter

  • Molecular and Cellular Biochemistry (Core)　D

    2022.12 - 2023.2   Winter quarter

  • 口腔生化学４

    2022.12 - 2023.2   Winter quarter

  • 口腔細胞工学（低年次）D

    2022.12 - 2023.2   Winter quarter

  • 口腔細胞工学（コア）D

    2022.12 - 2023.2   Winter quarter

  • 口腔細胞工学（高年次）C

    2022.10 - 2022.12   Fall quarter

  • 口腔脳機能病態学（低年次）　C

    2022.10 - 2022.12   Fall quarter

  • 口腔脳機能病態学（コア）　C

    2022.10 - 2022.12   Fall quarter

  • 口腔細胞工学（コア）　C

    2022.10 - 2022.12   Fall quarter

  • 口腔細胞工学（低年次）　C

    2022.10 - 2022.12   Fall quarter

  • Oral,Brain and Total Health Science (Core)　C

    2022.10 - 2022.12   Fall quarter

  • Molecular and Cellular Biochemistry (Lower-grade) C

    2022.10 - 2022.12   Fall quarter

  • Molecular and Cellular Biochemistry (Core)　C

    2022.10 - 2022.12   Fall quarter

  • 口腔生化学３

    2022.10 - 2022.12   Fall quarter

  • 口腔細胞工学（低年次）C

    2022.10 - 2022.12   Fall quarter

  • 口腔細胞工学（コア）C

    2022.10 - 2022.12   Fall quarter

  • 口腔細胞工学（高年次）B

    2022.6 - 2022.8   Summer quarter

  • 口腔脳機能病態学（低年次）　B

    2022.6 - 2022.8   Summer quarter

  • 口腔脳機能病態学（コア）　B

    2022.6 - 2022.8   Summer quarter

  • 口腔細胞工学（コア）　B

    2022.6 - 2022.8   Summer quarter

  • 口腔細胞工学（低年次）　B

    2022.6 - 2022.8   Summer quarter

  • Oral,Brain and Total Health Science (Core)　B

    2022.6 - 2022.8   Summer quarter

  • Molecular Cell Biology and Oral Anatomy (Lower-grade)　B

    2022.6 - 2022.8   Summer quarter

  • Molecular Cell Biology and Oral Anatomy (Core)　D

    2022.6 - 2022.8   Summer quarter

  • Molecular and Cellular Biochemistry (Lower-grade) B

    2022.6 - 2022.8   Summer quarter

  • Molecular and Cellular Biochemistry (Core)　B

    2022.6 - 2022.8   Summer quarter

  • 口腔生化学２

    2022.6 - 2022.8   Summer quarter

  • 口腔細胞工学（低年次）B

    2022.6 - 2022.8   Summer quarter

  • 口腔細胞工学（コア）B

    2022.6 - 2022.8   Summer quarter

  • Biochemistry and Biology

    2022.4 - 2023.3   Full year

  • 口腔細胞工学（高年次）A

    2022.4 - 2022.6   Spring quarter

  • 口腔脳機能病態学（低年次）　A

    2022.4 - 2022.6   Spring quarter

  • 口腔脳機能病態学（コア）　A

    2022.4 - 2022.6   Spring quarter

  • 口腔細胞工学（コア）　A

    2022.4 - 2022.6   Spring quarter

  • 口腔細胞工学（低年次）　A

    2022.4 - 2022.6   Spring quarter

  • Oral,Brain and Total Health Science (Core)　A

    2022.4 - 2022.6   Spring quarter

  • Molecular Cell Biology and Oral Anatomy (Lower-grade)　A

    2022.4 - 2022.6   Spring quarter

  • Molecular Cell Biology and Oral Anatomy (Core)　C

    2022.4 - 2022.6   Spring quarter

  • Molecular and Cellular Biochemistry (Lower-grade) A

    2022.4 - 2022.6   Spring quarter

  • Molecular and Cellular Biochemistry (Core)　A

    2022.4 - 2022.6   Spring quarter

  • 口腔生化学１

    2022.4 - 2022.6   Spring quarter

  • 口腔細胞工学（低年次）A

    2022.4 - 2022.6   Spring quarter

  • 口腔細胞工学（コア）A

    2022.4 - 2022.6   Spring quarter

  • Molecular and Cellular Biochemistry (Lower-grade) D

    2021.12 - 2022.2   Winter quarter

  • Molecular and Cellular Biochemistry (Lower-grade) C

    2021.10 - 2021.12   Fall quarter

  • 口腔細胞工学（低年次）　C

    2021.10 - 2021.12   Fall quarter

  • 口腔細胞工学（低年次）　D

    2021.10 - 2021.12   Fall quarter

  • Molecular and Cellular Biochemistry (Lower-grade) B

    2021.6 - 2021.8   Summer quarter

  • 口腔細胞工学（低年次）　B

    2021.6 - 2021.8   Summer quarter

  • 口腔生化学

    2021.4 - 2022.3   Full year

  • 生化学・口腔生化学

    2021.4 - 2022.3   Full year

  • 口腔細胞工学

    2021.4 - 2022.3   Full year

  • Biochemistry and Biology

    2021.4 - 2022.3   Full year

  • Introduction to Oral Biological Research（口腔細胞工学）

    2021.4 - 2022.3   Full year

  • Integrated Dental Science（口腔細胞工学）

    2021.4 - 2022.3   Full year

  • 歯学概論１

    2021.4 - 2021.9   First semester

  • Molecular and Cellular Biochemistry (Lower-grade) A

    2021.4 - 2021.6   Spring quarter

  • 口腔細胞工学（低年次）　A

    2021.4 - 2021.6   Spring quarter

  • 口腔細胞工学

    2020.4 - 2021.3   Full year

  • 生化学・口腔生化学

    2020.4 - 2021.3   Full year

  • 細胞の仕組み

    2020.4 - 2021.3   Full year

  • 口腔細胞工学

    2020.4 - 2021.3   Full year

  • 口腔細胞工学演習

    2020.4 - 2021.3   Full year

  • 細胞生物学特論

    2020.4 - 2021.3   Full year

  • Biochemistry and Biology

    2020.4 - 2021.3   Full year

  • 口腔常態制御学特論（口腔細胞工学）

    2020.4 - 2021.3   Full year

  • 口腔生化学

    2020.4 - 2021.3   Full year

  • 歯学概論１

    2020.4 - 2020.9   First semester

  • 口腔生化学

    2019.4 - 2020.3   Full year

  • 生化学・口腔生化学

    2019.4 - 2020.3   Full year

  • 細胞の仕組み

    2019.4 - 2020.3   Full year

  • 口腔細胞工学

    2019.4 - 2020.3   Full year

  • 口腔細胞工学演習

    2019.4 - 2020.3   Full year

  • Biochemistry and Biology

    2019.4 - 2020.3   Full year

  • 口腔細胞工学

    2019.4 - 2020.3   Full year

  • 口腔常態制御学研究入門（口腔細胞工学）

    2018.4 - 2019.3   Full year

  • 生化学・口腔生化学

    2018.4 - 2019.3   Full year

  • Biochemistry and Biology

    2018.4 - 2019.3   Full year

  • 細胞の仕組み

    2018.4 - 2019.3   Full year

  • 口腔細胞工学

    2018.4 - 2019.3   Full year

  • 口腔生化学

    2018.4 - 2019.3   Full year

  • 口腔細胞工学演習

    2018.4 - 2019.3   Full year

  • Biochemistry and Biology

    2018.4 - 2018.9   First semester

  • 口腔生化学

    2017.10 - 2018.3   Second semester

▼display all

FD Participation

  • 2024.7   Role：Planning   Title：入学者選抜における面接試験～位置付けと評価方法について

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

  • 2024.6   Role：Planning   Title：歯科医師国家試験合格率アップのための戦略

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

  • 2023.9   Role：Planning   Title：ハラスメントについて

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

  • 2023.6   Role：Planning   Title：科研費採択のためのFD

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

  • 2022.10   Role：Planning   Title：ゴミ廃棄について

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

  • 2022.5   Role：Planning   Title：科学研究費補助金採択率向上に向けて

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

  • 2018.5   Role：Participation   Title：臨床実習後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]

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

  • 2024  徳島大学歯学部  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2024  昭和大学　歯学部  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2024  福岡医健・スポーツ専門学校  Classification:Part-time lecturer 

  • 2023  昭和大学　歯学部  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2023  福岡医健・スポーツ専門学校  Classification:Part-time lecturer 

  • 2023  徳島大学歯学部  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2022  徳島大学　歯学部  Classification:Part-time lecturer 

  • 2022  福岡医健・スポーツ専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2021  福岡医健・スポーツ専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2021  昭和大学　歯学部  Classification:Part-time lecturer 

  • 2020  福岡医健・スポーツ専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2020  昭和大学　歯学部  Classification:Part-time faculty 

  • 2020  北九州小倉看護専門学校　准看護師科  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2019  福岡医健・スポーツ専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2019  九州歯科大学　歯学部  Classification:Part-time faculty 

  • 2019  昭和大学　歯学部  Classification:Part-time faculty 

  • 2019  北九州小倉看護専門学校　准看護師科  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2018  九州医療スポーツ専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2018  九州歯科大学　特任教授  Classification:Part-time faculty  Domestic/International Classification:Japan 

  • 2018  昭和大学歯学部  Classification:Part-time faculty  Domestic/International Classification:Japan 

  • 2018  北九州市小倉看護専門学校　准看護師科  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2017  九州医療スポーツ専門学校  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2017  九州歯科大学　特任教授  Classification:Part-time faculty  Domestic/International Classification:Japan 

  • 2017  昭和大学歯学部  Classification:Part-time faculty  Domestic/International Classification:Japan 

  • 2017  北九州小倉看護専門学校准看護師科  Classification:Part-time lecturer  Domestic/International Classification:Japan 

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Other educational activity and Special note

  • 2024  Class Teacher 

  • 2023  Class Teacher 

  • 2023  Special Affairs 

  • 2022  Class Teacher 

  • 2021  Class Teacher 

  • 2020  Class Teacher 

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Outline of Social Contribution and International Cooperation activities

  • Kyushu Clinical Regenerative Dentistry Research Association

Social Activities

  • 岩垂育英会　

    Role(s)： Advisor

    岩垂育英会　評議員  岩垂育英会  2024.6 - Present

    　More details

    Audience： Graduate students

    Type：Other

    将来歯科基礎医学分野のリーダーとなりうる優秀な大学院学生に奨学金援助を行うとともに、顕著な研究業績を挙げて活躍する基礎歯科医学研究者の顕彰をおこなう。

Media Coverage

  • 閉経後の骨量減・肥満解明 Newspaper, magazine

    日刊工業新聞  日刊工業新聞  2024.7

  • 口腔悪性黒色腫の浸潤　骨形成因子が関与 Newspaper, magazine

    日本歯科新聞  日本歯科新聞  2021.9

Activities contributing to policy formation, academic promotion, etc.

  • 2024.4 - 2025.3  

    歯科医師国家試験　試験委員

  • 2023.4 - 2024.3   厚生労働省

    歯科医師国家試験　試験委員

  • 2022.4 - 2023.3   厚生労働省

    歯科医師国家試験　試験委員

  • 2021.4 - 2022.3   厚生労働省

    歯科医師国家試験　試験委員

  • 2020.4 - 2021.3   厚生労働省

    歯科医師国家試験　試験委員

Acceptance of Foreign Researchers, etc.

  • 歯学研究院　口腔細胞工学分野

    Acceptance period： 2022.10 - 2026.9  

    Nationality：China

  • 九州大学歯学府

    Acceptance period： 2022.10 - 2026.9   （Period）：1 month or more

    Nationality：Bangladesh

    Business entity：Other

  • Acceptance period： 2022.10 - 2026.9   （Period）：1 month or more

    Business entity：Other

  • 歯学研究院　口腔細胞工学分野

    Acceptance period： 2022.4 - 2029.3   （Period）：1 month or more

    Nationality：China

  • 歯学研究院　口腔細胞工学分野

    Acceptance period： 2022.4 - 2026.3  

    Nationality：China

  • 歯学研究院　口腔細胞工学分野

    Acceptance period： 2021.4 - 2025.3  

    Nationality：China

  • 歯学研究院　口腔細胞工学分野

    Acceptance period： 2021.1 - 2026.9  

    Nationality：China

  • 歯学研究院　口腔細胞工学分野

    Acceptance period： 2019.10 - 2024.9   （Period）：1 month or more

    Nationality：China

    Business entity：Other

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Travel Abroad

  • 2024.10

    Staying countory name 1：Egypt   Staying institution name 1：National Research Center in Egypt

    Staying institution name 2：Ain Sham Univeristy

    Staying institution name 3：Cairo University

    Staying institution name (Other)：Alexandria University

  • 2023.2 - 2023.3

    Staying countory name 1：Indonesia   Staying institution name 1：Airlangga University

  • 2023.2

    Staying countory name 1：Korea, Republic of   Staying institution name 1：Pusan national University

  • 2011.11

    Staying countory name 1：China   Staying institution name 1：Beijing International Convention Center

  • 2011.2

    Staying countory name 1：Korea, Republic of   Staying institution name 1：Jukhyun Bio Auditorium, School of Life Science

  • 1998.10 - 2003.2

    Staying countory name 1：United States   Staying institution name 1：Division of Immunobiology, Yale University School of Medicine

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