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SHIMIZU Takeshi

    Graduate School of Medical Sciences Department of Neurophysiology and Brain Science　Lecturer
Last Updated :2024/04/12

Researcher Information

Research funding number

  • 60398237

J-Global ID

Profile

  • 2000 Graduated from Graduate School of Engineering Science, Osaka University. 2003 Graduated from the doctoral course at The Graduate University for Advanced Studies, School of Life Science, PhD. 2003 Postdoctoral Fellow, Institute of Molecular Embryology and Genetics, Kumamoto University. 2008 Postdoctoral Fellow, RIKEN CDB. 2010 Research Fellow, National University of Singapore, MechanoBiology Institute. 2012 Assistant Professor, NIPS

Research Interests

  • 幹細胞   メカノバイオロジー   GSK3β   神経前駆細胞   β-catenin   分化   細胞分裂   増殖   神経分化   oligodendrocyte   Wnt   glia   未分化性維持   神経幹細胞   細胞増殖   myelin   

Research Areas

  • Life sciences / Clinical pharmacy
  • Life sciences / Physiology
  • Life sciences / Neuroscience - general

Academic & Professional Experience

  • 2023/04 - Today  Shokei University短期大学部 食物栄養学科教授
  • 2017/08 - 2023/03  Nagoya City University医学研究科 脳神経生理学講師
  • 2012/04 - 2017/07  生理学研究所分子神経生理研究部門助教
  • 2010/04 - 2012/03  National University of SingaporeMechanobiology Institutepostdoctoral fellow
  • 2008/02 - 2010/03  理化学研究所 発生・再生科学総合研究センター体軸形成研究チーム研究員
  • 2003/04 - 2008/01  Kumamoto UniversityInstitute of Molecular Embryology and Geneticsポスドク

Education

  • 2000/04 - 2003/03  The Graduate University for Advanced Studies  School of Life Science  Department of Physiological Sciences
  • 1998/04 - 2000/03  Osaka University  基礎工学研究科 システム人間系  生物工学分野
  • 1994/04 - 1998/03  Osaka University  School of Engineering Science Direct Affiliates  生物工学科

Association Memberships

  • THE PHYSIOLOGICAL SOCIETY OF JAPAN   THE JAPANESE SOCIETY FOR NEUROCHEMISTRY   THE JAPAN NEUROSCIENCE SOCIETY   

Published Papers

Books etc

  • オリゴデンドロサイト-軸索相互作用による脳機能発現
    清水健史; 池中一裕 実験医学 第４章６ 169-174 2019/11
  • 神経系の分化、形成、再生
    田賀哲也; 鹿川哲史; 清水健史; 福田信治 分子生物学イラストレイテッド 改訂第3版 269-275

Conference Activities & Talks

  • Investigation of a novel mechanism underlying neuronal subtype-dependent myelination  [Not invited]
    清水健史; 村越秀治; 松本英俊; 長内康幸; 石田章真; 田尻直輝; 飛田秀樹
    日本生理学会 シンポジウム  2021/03
  • Mechanical control of oligodendrocyte morphogenesis and maturation by mechanosensors  [Not invited]
    Takeshi Shimizu; Yasuyuki Osanai; Kenji F Tanaka; Manabu Abe; Rie Natsume; Kenji Sakimura; Hideki Hida; Kazuhiro Ikenaka
    日本生理学会 一般口演  2018/03
  • Roles of oligodendrocyte-neuron interactions in myelination  [Invited]
    Takashi Shimizu; Yasuyuki Osanai; Kazuhiro Ikenaka
    日本神経化学会 シンポジウム  2017/09
  • Microglia-induced activation of non-canonical Wnt signaling aggravates neurodegeneration in demyelinating disorders  [Not invited]
    Takashi Shimizu; Ron Smits; Kazuhiro Ikenaka
    APSN, 14th Meeting of the Asian-Pacific Society for Neurochemistry  2016

MISC

  • 清水 健史; 長内 康幸; 池中 一裕  生化学  89-  (4)  559  -563  2017/08
  • K. Kunisawa; T. Shimizu; Y. Osanai; K. Kobayashi; A. Hayashi; H. Baba; M. A. Bhat; K. Ikenaka  JOURNAL OF NEUROCHEMISTRY  134-  286  -286  2015/08
  • 鹿川 哲史; 備前 典久; 清水 健史  生化学  86-  (1)  68  -71  2014/02
  • 神経幹/前駆細胞における細胞周期調節因子cyclin D1は細胞周期非依存的にアストロサイト分化を阻害する(Cyclin D1 inhibits astrocyte differentiation from neural stem/progenitor cells in a manner independent of cell cycle progression)
    備前 典久; 井上 俊洋; 清水 健史; 鹿川 哲史; 田賀 哲也  日本生化学会大会・日本分子生物学会年会合同大会講演要旨集  83回・33回-  3P  -0876  2010/12
  • Norihisa Bizen; Takeshi Shimizu; Toshihiro Inoue; Tetsushi Kagawa; Tetsuya Taga  DIFFERENTIATION  80-  S8  -S8  2010/11
  • 神経幹細胞/前駆細胞における細胞周期調節因子cyclin D1のアストロサイト分化抑制機構(Molecular mechanism underlying cyclin D1 mediated inhibition of astrocyte differentiation from neural stem/progenitor cells)
    備前 典久; 井上 俊洋; 清水 健史; 鹿川 哲史; 田賀 哲也  神経化学  49-  (2-3)  536  -536  2010/08
  • Norihisa Bizen; Toshihiro Inoue; Takeshi Shimizu; Tetsushi Kagawa; Tetsuya Taga  NEUROSCIENCE RESEARCH  68-  E132  -E132  2010
  • サイクリンD1は神経幹細胞/前駆細胞からの星状細胞分化を細胞周期調節非依存性に抑制する(Cyclin D1 inhibits astrocyte differentiation from neural stem/progenitor cells in a manner independent of cell cycle regulation)
    備前 典久; 井上 俊洋; 清水 健史; 鹿川 哲史; 田賀 哲也  神経化学  48-  (2-3)  205  -205  2009/06
  • 神経幹細胞画分における細胞周期調節因子cyclin D1はアストロサイト分化を阻害する(Cyclin D1 inhibits astrocyte differentiation in the section of neural stem cell)
    備前 典久; 井上 俊洋; 清水 健史; 鹿川 哲史; 田賀 哲也  神経化学  47-  (2-3)  245  -245  2008/08
  • Takeshi Shimizu; Masato Nakazawa; Tsutomu Hirata; Young-Ki Bae; Takashi Shimizu; Ryoichira Kageyama; Masahiko Hibi  NEUROSCIENCE RESEARCH  61-  S154  -S154  2008
  • 細胞増殖・細胞分化・細胞死・幹細胞 神経前駆細胞の増殖及び分化の調整におけるグリコーゲンシンターゼキナーゼ3βとβ-カテニンの役割(A Role for Glycogen Synthase Kinase 3beta and Beta-Catenin in Coordinating Proliferation and Differentiation of Neural Precursor Cells)
    清水 健史; 鹿川 哲史; 井上 俊洋; 高田 慎治; 田賀 哲也  日本発生生物学会・日本細胞生物学会合同大会要旨集  40回・59回-  61  -61  2007/05
  • 幹細胞制御の分子学的基礎 成長中のマウス脳における細胞運命決定の分子学的基礎(Molecular basis for stem cell regulation Molecular basis for cell-fate determination in the developing mouse brain)
    福田 信治; 清水 健史; 井上 俊洋; 鹿川 哲史; 田賀 哲也  日本発生生物学会・日本細胞生物学会合同大会要旨集  40回・59回-  23  -23  2007/05
  • T. Shimizu; T. Kagawa; T. Inoue; Y. Yoshinaga; S. Takada; T. Taga  INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE  24-  (8)  517  -517  2006/12
  • Wnt-3aは神経幹細胞の増殖と海馬発達に際しての神経細胞分化を共に促進する(Wnt-3a promotes both neural progenitor proliferation and neuronal differentiation during hippocampal development)
    鹿川 哲史; 吉永 豊; 清水 健史; 井上 俊洋; 田賀 哲也  神経化学  44-  (2-3)  184  -184  2005/08
  • 繊維芽細胞増殖因子2はグリコーゲン合成酵素キナーゼ3βを不活性化することによって未分化状体の神経幹細胞を維持し増殖を促進する(Fibroblast growth factor 2 maintains neural stem cells in an undifferentiated state and promotes their proliferation via the glycogen synthase kinase 3β inactivation)
    清水 健史; 鹿川 哲史; 井上 俊洋; 吉永 豊; 田賀 哲也  神経化学  44-  (2-3)  224  -224  2005/08
  • O Muraoka; T Yabe; T Shimizu; YK Bae; H Nojima; M Hibi  JOURNAL OF PHARMACOLOGICAL SCIENCES  97-  284P  -284P  2005
  • T Kagawa; A Nakahira; T Shimizu; K Ikenaka  JOURNAL OF NEUROCHEMISTRY  88-  12  -12  2004/02

Research Grants & Projects

  • オリゴデンドロサイトの力覚機構の解析と白質障害治療研究への応用
    日本学術振興会 科学研究費助成事業：基盤研究(C)
    Date (from‐to) : 2021/04 -2024/03 
    Author : 清水健史
  • Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research
    Date (from‐to) : 2018/04 -2022/03 
    Author : Hida Hideki
     
    Our final purpose is the establishment of cell therapy to perinatal white matter injury (PWMI). To establish cell therapy to a PWMI model rat using oligodendrocyte progenitor (OPC), we revealed that grafted OPC survived in the corpus callosum (CC) until 8week after the graft, and IGF-2 that is upregulated in the model brain exhibited trophic effect on cultured OPCs. Furthermore, to analyze the mechanism of the survival of the grafted cells in the CC, we performed several experiments focusing on the relationship between myelination and the recovery of the disturbed function: the analysis of myelin formation by FRET following to the construction of in vitro myelination system, and the analysis of the effect of environmental enrichment during the period of the development on the PWMI model.
  • Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research
    Date (from‐to) : 2015/11 -2018/03 
    Author : IKENAKA Kazuhiro; ITO Kei; UEKI Takatoshi; OHKI Kenichi; KATO Takahiro; KANEMARU Kazunori; SHIMIZU Takeshi; TAKEBAYASHI Hirohide; TANAKA Kenji; HASHIOTO Kohichi; YAMAZAKI Yoshihiko; INOUE Kazuhide; OKABE Shigeo; OZAKI Norio; KANBA Shigenobu; KIRA Junichi; KOHSAKA Shinichi; FUKUYAMA Hidenao; BANNAI Hiroko; NAKASHIMA Kinichi; IMAI Hiroo; MATSUI Ko; TACHIKAWA Masanori; KAKEGAWA Wataru
     
    We Glia Assembly communicated with Glial Heterogeneity (sponsored by DFG, program name SPP1757, project leader Dr. Frank Kirchhoff) and organized the international research consortium, called “YoungGlia”. The purpose of this framework is to stimulate mutual exchange visits of young researchers of glial research. The collaborative research between Japan and Germany will be carried out by the young researchers.The collaboration must be approved by the principle investigators on both sides but the original proposal and execution of the research itself must be done by the young researchers. According to the above basic concept, we selected 11 research pairs at 1st (FY2015) and 2nd (FY2016) YoungGlia and supported their international collaborations for 1-2 years. We organized 3rd YoungGlia (FY2017) and all funded pairs presented their achievements. In addition, at the 3rd YoungGlia, we invited Canadian and American groups and expanded our partnership beyond Japan-Germany communication.
  • Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research
    Date (from‐to) : 2013/06 -2018/03 
    Author : Ikenaka Kazuhiro
     
    Oligodendrocytes (OLs) have recently been shown to modulate conduction velocity in an axonal activity-dependent manner even after myelination is completed. The axonal activity also promotes the proliferation and differentiation of OL precursor cells, and these are required for motor skill learning. Taken together, these findings suggest that neuronal activity and subsequent myelin remodeling are required for executing higher brain function. We thus examined whether and/or how OLs play roles in higher brain functions, using following experimental systems. (1) A method for simultaneously labeling both axons from different brain regions and the myelinating OL, (2) Mouse lines with channelrhodopsin-2 expression in OL, (3) NF155 conditional knockout mice, whose paranodes are disrupted after their initial formation.
  • メカニカルストレスの生理的機能の解析
    日本学術振興会 科学研究費助成事業：挑戦的萌芽研究
    Date (from‐to) : 2016/04 -2018/03 
    Author : 清水健史
  • Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research
    Date (from‐to) : 2012/08 -2014/03 
    Author : SHIMIZU Takeshi
     
    Oligodendrocytes are glial cells that myelinate neuronal axons in the central nervous system. Myelin insulates axons to increase conduction velocity of neuronal action potentials. Recent studies have shown that mechanical factors influence various cell properties. Mechanical stimulation can be transduced to intracellular biochemical signals through conformational changes in focal adhesion-related mechanosensors. We analyzed oligodendrocyte morphology and myelination in relation with the mechanosensors. In addition, we found that non-canonical Wnt signaling was up-regulated in a demyelinating mouse model. We examined whether non-canonical Wnt signaling pathway had a role in the Experimental Autoimmune Encephalomyelitis-induced neural pathology.
  • 日本学術振興会：科学研究費助成事業
    Date (from‐to) : 2006 -2007 
    Author : 清水 健史
     
    増殖と分化の相反する性質は一般的な細胞系譜制御の根本原理のーつである。すなわち増殖の盛んな中枢神経系前駆細胞は未分化状態を保ったまま数を増やすが、ひとたび細胞周期をはずれた前駆細胞はニューロンやグリアへと分化する。しかしながら、増殖と分化を同調させる分子メカニズムについて未だ不明な点が多い。神経幹細胞を再生医療で使用する際に、細胞数とニューロンへの分化をコントロールする上で、その分子メカニズムの理解は重要である。昨年度までに我々は、FGF2シグナルによって神経上皮細胞の増殖が促進される際に働く主要な経路として、PI3K-Akt経路を介したGSK3βの不活性化によるCyclinD1の発現上昇を明らかにしてきた。またFGF2が細胞の未分化性を維持する分子メカニズムとして、PI3K-Akt-GSK3β経路を介して、Notchシグナルの標的であるHes遺伝子発現を増強し、細胞分化抑制に働くことを見出した。平成19年度には、我々は新たにGSK3βの不活化の後、β-cateninタンパク質がNotch1細胞内領域と直接相互作用することを見い出した。その際、β-cateninとNotch1細胞内領域の複合体は、転写のcoactivatorであるp300やP/CAFとも結合し、その結果Hes1プロモーターが活性化される分子機構を新たに明らかにした。またクロマチン免疫沈降法によって、β-cateninタンパク質が実際にHes1プロモーターに結合することを確かめた。次に、生体内における細胞系譜への影響を調べる目的で、子宮内電気穿孔法を用いてGSK3の機能を解析した。その結果、GSK3ノックダウン細胞が脳室周囲に限局したことから、GSK3が神経前駆細胞の未分化性維持を制御する可能性が示唆された。これらの結果から、増殖と分化を同調させる分子メカニズムのーつが明らかになった。
  • Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research
    Date (from‐to) : 2005 -2006 
    Author : KAGAWA Tetsushi; SHIMIZU Takashi
     
    The effects of Wnt signaling on neural progenitor cells were controversial: it was reported to either promote their cell proliferation or accelerate differentiation to become postmitotic neurons. To understand this discrepant role of the Wnt canonical pathway, we applied Wnt3a on the primary culture prepared from embryonic day 15 mouse hippocampus. Wnt3a increased the numbers of total cells, proliferating cells and differentiated neurons. This result phenomenologically suggests that Wnt3a induces both neural progenitor cell proliferation and neuronal differentiation. Notably, the ratio of the number of neurons to total cells after the culture was almost comparable. Wnt3a did not significantly affect the ratio of symmetric and asymmetric cell divisions, but accelerated cell cycle progression by shortening the cell cycle duration, which could result in increases of both proliferative cells and differentiated neurons.

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