Updated on 2025/02/22

写真a

 
HATTORI Takako
 
Organization
Faculty of Medicine, Dentistry and Pharmaceutical Sciences Assistant Professor
Position
Assistant Professor
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Degree

  • 博士(歯学) ( 岡山大学 )

Research Interests

  • 分子生物学

  • 口腔生化学

  • 関節リウマチ

  • 発生生物学

  • cell biology

  • transcriptional control

  • bone

  • circadian rhythm

  • Sox9

  • CCN family proteins

  • osteoarthritis

  • articular cartilage

  • anti-aging

  • endochondral bone formation

  • cartilage

  • 時計遺伝子

  • 老化

  • トランスクリプトーム解析

Research Areas

  • Life Science / Oral biological science  / Oral biochemistry

  • Life Science / Molecular biology

  • Life Science / Oral pathobiological science

  • Life Science / Cell biology

Education

  • Okayama University   理学部   生物

    - 1990

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    Country: Japan

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  • 岡山大学大学院   歯学研究科  

    2000.9

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    Notes: 博士(歯学)

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Research History

  • Department of Orthopaedics, University of Maryland School of Medicine(米国)

    2023.2 - 2023.3

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    Country:United States

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  • - Assistant Professor,Graduate School of Medicine, Dentistry and Pharmaceutical Sciences,Okayama University

    2004

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  • - 岡山大学医歯薬学総合研究科 助教

    2004

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  • Researcher,Department of Molecular Genetics, MD Anderson Cancer Center, The University of Texas

    2001 - 2004

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Professional Memberships

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Committee Memberships

  •   岡山大学臨床研究審査専門委員会委員  

    2021.4   

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    Committee type:Other

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  •   歯学部将来構想検討WG委員  

    2018.4   

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  •   安全衛生委員会作業部会委員  

    2017.4   

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  •   国際交流部会副部会長  

    2015.4   

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  •   OSCE実行委員会委員  

    2006.4   

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Papers

  • Do not overwork: cellular communication network factor 3 for life in cartilage. Reviewed International journal

    Satoshi Kubota, Harumi Kawaki, Bernard Perbal, Masaharu Takigawa, Kazumi Kawata, Takako Hattori, Takashi Nishida

    Journal of cell communication and signaling   17 ( 2 )   353 - 359   2023.6

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

    Cellular communication network factor (CCN) 3, which is one of the founding members of the CCN family, displays diverse functions. However, this protein generally represses the proliferation of a variety of cells. Along with skeletal development, CCN3 is produced in cartilaginous anlagen, growth plate cartilage and epiphysial cartilage. Interestingly, CCN3 is drastically induced in the growth plates of mice lacking CCN2, which promotes endochondral ossification. Notably, chondrocytes in these mutant mice with elevated CCN3 production also suffer from impaired glycolysis and energy metabolism, suggesting a critical role of CCN3 in cartilage metabolism. Recently, CCN3 was found to be strongly induced by impaired glycolysis, and in our study, we located an enhancer that mediated CCN3 regulation via starvation. Subsequent investigations specified regulatory factor binding to the X-box 1 (RFX1) as a transcription factor mediating this CCN3 regulation. Impaired glycolysis is a serious problem, resulting in an energy shortage in cartilage without vasculature. CCN3 produced under such starved conditions restricts energy consumption by repressing cell proliferation, leading chondrocytes to quiescence and survival. This CCN3 regulatory system is indicated to play an important role in articular cartilage maintenance, as well as in skeletal development. Furthermore, CCN3 continues to regulate cartilage metabolism even during the aging process, probably utilizing this regulatory system. Altogether, CCN3 seems to prevent "overwork" by chondrocytes to ensure their sustainable life in cartilage by sensing energy metabolism. Similar roles are suspected to exist in relation to systemic metabolism, since CCN3 is found in the bloodstream.

    DOI: 10.1007/s12079-023-00723-4

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  • Elevated Expression of CCN3 in Articular Cartilage Induces Osteoarthritis in Hip Joints Irrespective of Age and Weight Bearing. Reviewed International journal

    Kazuki Hirose, Miho Kuwahara, Eiji Nakata, Tomonori Tetsunaga, Kazuki Yamada, Kenta Saiga, Masaharu Takigawa, Toshifumi Ozaki, Satoshi Kubota, Takako Hattori

    International journal of molecular sciences   23 ( 23 )   2022.12

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    Osteoarthritis (OA) occurs not only in the knee but also in peripheral joints throughout the whole body. Previously, we have shown that the expression of cellular communication network factor 3 (CCN3), a matricellular protein, increases with age in knee articular cartilage, and the misexpression of CCN3 in cartilage induces senescence-associated secretory phenotype (SASP) factors, indicating that CCN3 promotes cartilage senescence. Here, we investigated the correlation between CCN3 expression and OA degenerative changes, principally in human femoral head cartilage. Human femoral heads obtained from patients who received total hip arthroplasty were categorized into OA and femoral neck fracture (normal) groups without significant age differences. Gene expression analysis of RNA obtained from femoral head cartilage revealed that CCN3 and MMP-13 expression in the non-weight-bearing part was significantly higher in the OA group than in the normal group, whereas the weight-bearing OA parts and normal cartilage showed no significant differences in the expression of these genes. The expression of COL10A1, however, was significantly higher in weight-bearing OA parts compared with normal weight-bearing parts, and was also higher in weight-bearing parts compared with non-weight-bearing parts in the OA group. In contrast, OA primary chondrocytes from weight-bearing parts showed higher expression of CCN3, p16, ADAMTS4, and IL-1β than chondrocytes from the corresponding normal group, and higher ADAMTS4 and IL-1β in the non-weight-bearing part compared with the corresponding normal group. Acan expression was significantly lower in the non-weight-bearing group in OA primary chondrocytes than in the corresponding normal chondrocytes. The expression level of CCN3 did not show significant differences between the weight-bearing part and non-weight-bearing part in both OA and normal primary chondrocytes. Immunohistochemical analysis showed accumulated CCN3 and aggrecan neoepitope staining in both the weight-bearing part and non-weight-bearing part in the OA group compared with the normal group. The CCN3 expression level in cartilage had a positive correlation with the Mankin score. X-ray analysis of cartilage-specific CCN3 overexpression mice (Tg) revealed deformation of the femoral and humeral head in the early stage, and immunohistochemical analysis showed accumulated aggrecan neoepitope staining as well as CCN3 staining and the roughening of the joint surface in Tg femoral and humeral heads. Primary chondrocytes from the Tg femoral head showed enhanced expression of Ccn3, Adamts5, p16, Il-6, and Tnfα, and decreased expression of Col2a1 and -an. These findings indicate a correlation between OA degenerative changes and the expression of CCN3, irrespective of age and mechanical loading. Furthermore, the Mankin score indicates that the expression level of Ccn3 correlates with the progression of OA.

    DOI: 10.3390/ijms232315311

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  • Molecular and Genetic Interactions between CCN2 and CCN3 behind Their Yin-Yang Collaboration. Reviewed International journal

    Satoshi Kubota, Kazumi Kawata, Takako Hattori, Takashi Nishida

    International journal of molecular sciences   23 ( 11 )   2022.5

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    Cellular communication network factor (CCN) 2 and 3 are the members of the CCN family that conduct the harmonized development of a variety of tissues and organs under interaction with multiple biomolecules in the microenvironment. Despite their striking structural similarities, these two members show contrastive molecular functions as well as temporospatial emergence in living tissues. Typically, CCN2 promotes cell growth, whereas CCN3 restrains it. Where CCN2 is produced, CCN3 disappears. Nevertheless, these two proteins collaborate together to execute their mission in a yin-yang fashion. The apparent functional counteractions of CCN2 and CCN3 can be ascribed to their direct molecular interaction and interference over the cofactors that are shared by the two. Recent studies have revealed the mutual negative regulation systems between CCN2 and CCN3. Moreover, the simultaneous and bidirectional regulatory system of CCN2 and CCN3 is also being clarified. It is of particular note that these regulations were found to be closely associated with glycolysis, a fundamental procedure of energy metabolism. Here, the molecular interplay and metabolic gene regulation that enable the yin-yang collaboration of CCN2 and CCN3 typically found in cartilage development/regeneration and fibrosis are described.

    DOI: 10.3390/ijms23115887

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  • Maternal Gut Microbiome Decelerates Fetal Endochondral Bone Formation by Inducing Inflammatory Reaction. Reviewed International journal

    Yoko Uchida-Fukuhara, Takako Hattori, Shanqi Fu, Sei Kondo, Miho Kuwahara, Daiki Fukuhara, Md Monirul Islam, Kota Kataoka, Daisuke Ekuni, Satoshi Kubota, Manabu Morita, Mika Iikegame, Hirohiko Okamura

    Microorganisms   10 ( 5 )   2022.5

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    To investigate the effect of the maternal gut microbiome on fetal endochondral bone formation, fetuses at embryonic day 18 were obtained from germ-free (GF) and specific-pathogen-free (SPF) pregnant mothers. Skeletal preparation of the fetuses' whole bodies did not show significant morphological alterations; however, micro-CT analysis of the tibiae showed a lower bone volume fraction in the SPF tibia. Primary cultured chondrocytes from fetal SPF rib cages showed a lower cell proliferation and lower accumulation of the extracellular matrix. RNA-sequencing analysis showed the induction of inflammation-associated genes such as the interleukin (IL) 17 receptor, IL 6, and immune-response genes in SPF chondrocytes. These data indicate that the maternal gut microbiome in SPF mice affects fetal embryonic endochondral ossification, possibly by changing the expression of genes related to inflammation and the immune response in fetal cartilage. The gut microbiome may modify endochondral ossification in the fetal chondrocytes passing through the placenta.

    DOI: 10.3390/microorganisms10051000

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  • Cysteinyl leukotriene receptor 1 is dispensable for osteoclast differentiation and bone resorption. Reviewed International journal

    Hirofumi Fujita, Aoi Ando, Yohei Mizusawa, Mitsuaki Ono, Takako Hattori, Munenori Habuta, Toshitaka Oohashi, Satoshi Kubota, Hideyo Ohuchi

    PloS one   17 ( 11 )   e0277307   2022

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    Cysteinyl leukotriene receptor 1 (CysLTR1) is a G protein-coupled receptor for the inflammatory lipid mediators cysteinyl leukotrienes, which are involved in smooth muscle constriction, vascular permeability, and macrophage chemokine release. The Cysltr1 gene encoding CysLTR1 is expressed in the macrophage lineage, including osteoclasts, and the CysLTR1 antagonist Montelukast has been shown to suppress the formation of osteoclasts. However, it currently remains unclear whether CysLTR1 is involved in osteoclast differentiation and bone loss. Therefore, to clarify the role of CysLTR1 in osteoclastogenesis and pathological bone loss, we herein generated CysLTR1 loss-of-function mutant mice by disrupting the cysltr1 gene using the CRISPR-Cas9 system. These mutant mice had a frameshift mutation resulting in a premature stop codon (Cysltr1 KO) or an in-frame mutation causing the deletion of the first extracellular loop (Cysltr1Δ105). Bone marrow macrophages (BMM) from these mutant mice lost the intracellular flux of calcium in response to leukotriene D4, indicating that these mutants completely lost the activity of CysLTR1 without triggering genetic compensation. However, disruption of the Cysltr1 gene did not suppress the formation of osteoclasts from BMM in vitro. We also demonstrated that the CysLTR1 antagonist Montelukast suppressed the formation of osteoclasts without functional CysLTR1. On the other hand, disruption of the Cysltr1 gene partially suppressed the formation of osteoclasts stimulated by leukotriene D4 and did not inhibit that by glutathione, functioning as a substrate in the synthesis of cysteinyl leukotrienes. Disruption of the Cysltr1 gene did not affect ovariectomy-induced osteoporosis or lipopolysaccharide-induced bone resorption. Collectively, these results suggest that the CysLT-CysLTR1 axis is dispensable for osteoclast differentiation in vitro and pathological bone loss, while the leukotriene D4-CysTR1 axis is sufficient to stimulate osteoclast formation. We concluded that the effects of glutathione and Montelukast on osteoclast formation were independent of CysLTR1.

    DOI: 10.1371/journal.pone.0277307

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Books

  • Molecular and Genetic Interactions between CCN2 and CCN3 behind Their Yin-Yang Collaboration.

    Kubota S, Kawata K, Hattori T, Nishida T( Role: Joint author)

    Int J Mol Sci., MDPI  2022 

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  • Cellular communication network factor 3 in cartilage development and maintenance.

    Kubota S, Kawaki H, Perbal B, Kawata K, Hattori T, Nishida T( Role: Joint author)

    J Cell Commun. Signal.  2021 

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  • Retrotransposons Manipulating Mammalian Skeletal Development in Chondrocytes

    Kubota S, Ishikawa T, Kawata K, Hattori T, Nishida T.( Role: Joint author)

    Int J Mol Sci., MDPI  2020.2 

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  • 低身長治療のみでなく関節機能維持によるアンチエイジング療法の開発を目的とした軟骨組織の概日リズム形成機構の解明

    ( Role: Sole author)

    一般社団法人至誠会  2019.4 

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    Language:Japanese

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  • New function of Tip60 in controlling triacylglycerol synthesis.

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    Biotarget  2018.9 

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MISC

  • 霊長類特異的long non coding urothelial cancer associated 1 (UCA1)のCRISPR-CAS9を用いたknock-inマウスの作製とその解析。

    近藤 星, 桑原実穂, Shanqi, Fu, Kavitha, Panneer Selvam, Janvier Habumugisha, 大野充昭, 藤井匡寛, 西田 崇, 久保田聡, 服部高子

    第97回日本生化学会年会   2024.11

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  • 霊長類特異的long non coding RNA, urothelial cancer associated 1のCRISPR-CAS9を用いたknock-inマウスの作製とゲノム中でのUCA1の不安定性

    近藤 星, 桑原実穂, Fu Shanqi, Selvam Kavitha Panneer, Janvier Habumugisha, 大野充昭, 藤井匡寛, 西田 崇, 久保田聡, 服部高子

    第47回日本分子生物学会年会   2024.11

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  • 軟骨組織においてCCN3は加齢に伴って発現上昇するが,その発現上昇は,年齢,荷重の有無に関わらず軟骨変性度と相関する

    服部高子, 桑原実穂, 廣瀬一樹, 近藤星, FU Shanqi, 滝川正春, 久保田聡

    日本骨代謝学会学術集会プログラム抄録集(CD-ROM)   42nd   2024

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  • CCN3, a senescence marker of cartilage, correlate with osteoarthritis irrespective of age and weight bearing

    桑原実穂, 廣瀬一樹, 廣瀬一樹, 奥田龍一郎, HABUMUGISHA Janvier, 近藤星, FU Shanqi, 大野充昭, 古松毅之, 中田英二, 滝川正春, 久保田聡, 服部高子

    日本分子生物学会年会プログラム・要旨集(Web)   46th   2023.12

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  • 軟骨組織の加齢とともに発現が上昇するCCN3は、その発現上昇と軟骨変性度が年齢、荷重の有無に関わらず相関する

    桑原 実穂, 廣瀬 一樹, 近藤 星, Fu Shanqi, 大野 充昭, 古松 毅之, 中田 英二, 滝川 正春, 久保田 聡, 服部 高子

    第96回日本生化学会大会   96回   [2P - 516]   2023.11

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    Authorship:Last author, Corresponding author   Language:Japanese   Publisher:(公社)日本生化学会  

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Presentations

  • 霊長類特異的long non coding urothelial cancer associated 1 (UCA1)のCRISPR-CAS9を用いたknock-inマウスの作製とその解析。

    近藤 星, 桑原実穂, Shanqi, Fu, Kavitha, Panneer Selvam, Janvier Habumugisha, 大野充昭, 藤井匡寛, 西田 崇, 久保田聡, 服部高子

    第97回日本生化学会年会  2024.11 

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    Event date: 2024.11

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  • 霊長類特異的long non coding RNA, urothelial cancer associated 1のCRISPR-CAS9を用いたknock-inマウスの作製とゲノム中でのUCA1の不安定性

    近藤 星, 桑原実穂, Fu Shanqi, Selvam Kavitha Panneer, Janvier Habumugisha, 大野充昭, 藤井匡寛, 西田 崇, 久保田聡, 服部高子

    第47回日本分子生物学会年会  2024.11 

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    Event date: 2024.11

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  • 軟骨組織においてCCN3は加齢に伴って発現上昇するが,その発現上昇は,年齢,荷重の有無に関わらず軟骨変性度と相関する

    服部高子, 桑原実穂, 廣瀬一樹, 近藤星, FU Shanqi, 滝川正春, 久保田聡

    日本骨代謝学会学術集会プログラム抄録集(CD-ROM)  2024 

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    Event date: 2024

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  • 軟⾻組織においてCCN3の発現上昇は、年齢、荷重の有無に関わらず軟⾻ 変性度と相関する

    桑原 実穂, 廣瀬 一樹, 奥田 龍一郎, Janvier Habumugisha, 近藤 星, Shanqi Fu, 大野 充昭, 古松毅之, 中田 英二, 滝川 正春, 久保田 聡, 服部 高子

    第46回日本分子生物学会年会  2023.12.6 

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    Event date: 2023.12.6 - 2023.12.8

    Presentation type:Symposium, workshop panel (public)  

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  • 軟骨組織の加齢とともに発現が上昇するCCN3は、その発現上昇と軟骨変性度が年齢、荷重の有無に関わらず相関する

    桑原 実穂, 廣瀬 一樹, 近藤 星, Fu Shanqi, 大野 充昭, 古松 毅之, 中田 英二, 滝川 正春, 久保田 聡, 服部 高子

    第96回日本生化学会大会  2023.10.31 

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    Event date: 2023.10.31 - 2023.11.2

    Presentation type:Poster presentation  

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Industrial property rights

  • がんの治療又は予防剤

    滝川 正春, 服部 高子, 皆川 吉, 瀬戸 泰裕, 綱 美香, 原田 義孝, 高久 学, 安田 秀世

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    Applicant:日本製粉株式会社, 国立大学法人 岡山大学

    Application no:特願2013-006973  Date applied:2013.1.18

    Announcement no:特開2013-166751  Date announced:2013.8.29

    J-GLOBAL

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  • がんの治療又は予防剤

    滝川 正春, 服部 高子, 皆川 吉, 瀬戸 泰裕, 綱 美香, 原田 義孝, 高久 学, 安田 秀世

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    Applicant:日本製粉株式会社, 国立大学法人 岡山大学

    Application no:特願2013-006973  Date applied:2013.1.18

    Announcement no:特開2013-166751  Date announced:2013.8.29

    Patent/Registration no:特許第6187960号  Date registered:2017.8.10  Date issued:2017.8.10

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Works

  • 第43回岡山歯学会・学術集会、岡山歯学会優秀論文賞: Roles of interaction between CCN2 and Rab14 in aggrecan production by chondrocytes.

    Hoshijima, M, Hattori, T, Aoyama, E, Nishida, T, Kubota, S, Takigawa, M

    2022.12.11

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  • 第45回日本分子生物学会 日本生物物理学会 共催、サイエンスピッチアワード・優秀発表賞: 軟骨細胞におけるメトホルミンによるlong non-coding RNA, UCA1およびCCN2の発現制御

    近藤 星, 服部高子, 桑原実穂, Fu Shanqi, 西田 崇, 薬師寺翔太, 吉岡洋祐, 森谷徳文, 飯田征二, 滝川正春, 久保田聡

    2022.12.2

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  • 第42回岡山歯学会・学術集会、岡山歯学会奨励論文賞

    Fu Shanqi, Kuwahara Miho, Uchida Yoko, Kondo Sei, Nishida Takashi, Ikegame Mika, Maruyama Yusuke, Hattori Atsuhiko, Takagaki Asami, Shimomura Yuji, Hayashi Daichi, Kubota Satoshi, Hattori Takako

    2021.10.28

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  • 第91回日本生化学会大会若手優秀発表賞

    Shanqi Fu, 桑原 実穂, 内田 瑶子, 林 大智, 下村 侑司, 高垣 安紗美, 西田 崇, 丸山 雄介, 池亀 美華, 服部 淳彦, 服部 高子, 久保田 聡

    2018.9.24
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    2018.9.26

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  • 平成29年度至誠会基礎医学研究助成渡辺慶子賞

    服部高子

    2017

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Awards

  • 岡山歯学会優秀論文賞

    2022.12  

    Hoshijima, M, Hattori, T, Aoyama, E, Nishida, T, Kubota, S, Takigawa, M

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  • サイエンスピッチアワード・優秀発表賞

    2022.12   日本分子生物学会 日本生物物理学会共催   軟骨細胞におけるメトホルミンによるlong non-coding RNA, UCA1およびCCN2の発現制御

    近藤 星、 服部高子、桑原実穂、Fu Shanqi、西田 崇、薬師寺翔太、吉岡洋祐、森谷徳文、飯田征二、滝川正春、久保田聡

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  • 岡山歯学会奨励論文賞

    2021.11   岡山歯学会  

    Fu Shanqi, Kuwahara Miho, Uchida Yoko, Kondo Sei, Nishida Takashi, Ikegame Mika, Maruyama Yusuke, Hattori Atsuhiko, Takagaki Asami, Shimomura Yuji, Hayashi Daichi, Kubota Satoshi, Hattori Takako

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  • 第91回日本生化学会大会若手優秀発表賞

    2018.9   日本生化学会大会  

    Shanqi Fu, 桑原 実穂, 内田 瑶子, 林 大智, 下村 侑司, 高垣 安紗美, 西田 崇, 丸山 雄介, 池亀 美華, 服部 淳彦, 服部 高子, 久保田 聡

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  • 平成29年度至誠会基礎医学研究助成渡辺慶子賞

    2017   一般社団法人 至誠会   低身長治療のみでなく関節機能維持によるアンチエイジング療法の開発を目的とした軟骨組織の概日リズム形成機構の解明

    服部高子

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Research Projects

  • 糖代謝障害が招く軟骨肥大性細胞老化を介したO Aの発症機構の解明とC C N2の役割

    Grant number:24K12869  2024.04 - 2027.03

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    西田 崇, 服部 高子, 青山 絵理子, 高江洲 かずみ, 滝川 正春, 久保田 聡

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    Grant amount:\4550000 ( Direct expense: \3500000 、 Indirect expense:\1050000 )

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  • Investigation on phase separation-mediated regulation of cell differentiation by droplet transpricptomics

    Grant number:24H00652  2024.04 - 2027.03

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

    久保田 聡, 西田 崇, 服部 高子, 高江洲 かずみ, 滝川 正春, 青山 絵理子, 大野 充昭

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    Grant amount:\48100000 ( Direct expense: \37000000 、 Indirect expense:\11100000 )

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  • 下顎頭軟骨変性を制御する分子メカニズムの解明

    Grant number:24K13004  2024.04 - 2027.03

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    桑原 実穂, 原 哲也, 丸尾 幸憲, 服部 高子, 角谷 宏一

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    Grant amount:\4680000 ( Direct expense: \3600000 、 Indirect expense:\1080000 )

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  • Development of dropletomics that clarifies transcriptional regulation under liquid-liquid phase separation

    Grant number:23K17439  2023.06 - 2027.03

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

    久保田 聡, 西田 崇, 服部 高子, 高江洲 かずみ, 滝川 正春, 青山 絵理子, 大野 充昭

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    Grant amount:\25740000 ( Direct expense: \19800000 、 Indirect expense:\5940000 )

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  • 象牙芽細胞の表面に突き出た細胞小器官の機能解析と象牙質再生への応用

    Grant number:22K10075  2022.04 - 2025.03

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    高江洲 かずみ, 服部 高子, 青山 絵理子, 滝川 正春, 西田 崇, 久保田 聡

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    Grant amount:\4290000 ( Direct expense: \3300000 、 Indirect expense:\990000 )

    象牙芽細胞の一次繊毛の形成や細胞周期制御に機能するIntraflagellar transport (Ift) 88の機能制御により、理想的な形質・形態の象牙質の再生を目指すべく、まずは正常象牙質の形成過程である1. 象牙芽前駆細胞の接着・増殖、2. 分化、3. 細胞極性の分子制御機構の検討を行っている。
    現在までに、IFT88は古典的WNTシグナルの抑制を介して象牙芽細胞分化を制御すること、また、古典的WNTシグナルは一次繊毛形成を抑制することを明らかにしている(Bone, 2021)。
    本研究では、細胞増殖速度への影響を検討しており、Ift88をノックダウンしたsh-Ift88 MRMT-1細胞(乳癌細胞株)では、現在までの報告通り増加したが、Ift88をノックダウンしたsh-Ift88 KN-3細胞(象牙芽前駆細胞)では抑制された。この制御機構を探索するために、細胞増殖制御に機能するHippoシグナル経路の転写共役因子YAPの核移行検討について検討を行った。その結果、sh-Ift88 MRMT-1細胞においてはYAPが核移行する細胞数は増加したが、sh-Ift88 KN-3細胞ではYAPが核移行する細胞数は増加と減少の二極性を示した。また、Hippoシグナル経路とクロストークするWNTシグナル経路の転写調節因子beta-cateninの核移行についても同様に検討を行った。その結果、sh-Ift88 MRMT-1細胞においては、beta-cateninが核移行する細胞数は増加したが、sh-Ift88 KN-3細胞では減少した。現在は、それぞれのシグナルのactivator, inhibitorを添加し、その影響を検討中である。

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Class subject in charge

  • Internal Medicine (2024academic year) 1st and 2nd semester  - [第1学期]月4,月5,水6, [第2学期]月4,月5,金6

  • From molecules to organisms (2024academic year) Third semester  - 金5~6

  • Molecular Dentistry (2024academic year) 3rd and 4th semester  - [第3学期]水4, [第4学期]月4

  • Molecular Biology and Biochemistry of Signal Transduction (2024academic year) Second semester  - 木1,木2,木3

  • Molecular Dentistry Demonstration (2024academic year) Fourth semester  - 水4,水5,水6,水7,木1,木2,木3

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Media Coverage

  • 細胞外マトリックスから見た老化研究 Newspaper, magazine

    科学新聞  日本分子生物学会年会注目シンポジウム  2024.1

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  • 軟骨細胞におけるメトホルミンによるlong non-coding RNA, UCA1およびCCN2の発現制御 Promotional material

    第45回日本分子生物学会 日本生物物理学会 共催、サイエンスピッチアワード・優秀発表賞  2022.12

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  • 低身長治療のみでなく関節機能維持によるアンチエイジング療法の開発を目的とした軟骨組織の概日リズム形成機構の解明 Promotional material

    一般社団法人至誠会 基礎医学研究助成 渡辺慶子賞 研究報告書  2019

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  • 常在菌が正常な骨形成を促進するメカニズムを発見 Promotional material

    岡山大学ホームページ  2018.9

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  • CCNファミリーメンバー2/結合組織成長因子(CCN2/CTGF)の軟骨組織特異的過剰発現はインスリン様成長因子の発現と骨の成長を誘発する Internet

    1st Author, 日本骨代謝学会ホームページ  2014

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    Author:Myself 

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Academic Activities

  • 第43回岡山歯学会総会・学術集会

    Role(s):Planning, management, etc., Planning/Implementing academic research

    2022.12.11

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    Type:Academic society, research group, etc. 

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  • 生命倫理委員会臨床研究審査専門委員会

    Role(s):Peer review

    申請のあった臨床研究の整合性を判断する。  2020.4

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    Type:Scientific advice/Review 

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