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Analysis of the contribution of satellite cells to sarcopenia

Research Project

Project/Area Number 19K07396
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 49010:Pathological biochemistry-related
Research InstitutionTokyo Medical and Dental University

Principal Investigator

Matsuzaki Kyoko  東京医科歯科大学, 大学院医歯学総合研究科, 助教 (90568932)

Project Period (FY) 2019-04-01 – 2023-03-31
Project Status Completed (Fiscal Year 2022)
Budget Amount *help
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2021: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Keywordsサテライト細胞 / サルコペニア / 老化
Outline of Research at the Start

本研究では、骨格筋組織幹細胞(サテライト細胞)がサルコペニア治療の新たな標的となり得るかを明らかにするため、早老症モデルHGPSマウスを用いてサテライト細胞の量的および質的な加齢性変化を検証する。特に運動(機械刺激)によるheterochromatin構造の変化に着目し、サテライト細胞において、機械刺激に応答してheterochromatinからeuchromatinへ移行する遺伝子を探索する。
さらに、それらの遺伝子のうちHGPSマウス由来の細胞では移行が見られなくなるもの、すなわち加齢に伴って運動負荷による応答性を失う遺伝子を選出し、サルコペニア治療の直接の標的候補を探索する。

Outline of Final Research Achievements

In this study, I focused on age-related changes in skeletal muscle tissue stem cells (satellite cells) as a new target for the treatment of sarcopenia. By isolating satellite cells from HGPS mice, a mouse model that mimics human progeria, it was clarified that satellite cells lose stemness and proliferative ability with aging. Furthermore, I found that the decrease of Myc signal is one of the causes of diminished proliferative capacity.
In addition, considering that it is important to restore the proliferative ability of satellite cells as a method of preventing and treating sarcopenia, I screened a library of low-molecular-weight compounds and identified several candidate compounds that promote the proliferative ability of satellite cells.

Academic Significance and Societal Importance of the Research Achievements

サルコペニアは高齢者が要介護になる主要な背景病態の一つであり、少子高齢化が進み、労働人口が減少する日本にとってサルコペニア対策は重要な政策課題である。サルコペニアを予防、治療するためには病態機構の解析が必須であるが、その詳細には不明な点が多く効果的な薬剤は未だ開発されていない。
本研究では、サテライト細胞が加齢に伴い質的に変化することを見出し、サテライト細胞がサルコペニアの発症に強く関わっていることを示唆した。したがって、サテライト細胞がサルコペニア治療の有望なターゲットになると期待され、その社会的意義は大きい。

Report

(5 results)
  • 2022 Annual Research Report   Final Research Report ( PDF )
  • 2021 Research-status Report
  • 2020 Research-status Report
  • 2019 Research-status Report
  • Research Products

    (8 results)

All 2022 2021 2020 2019

All Journal Article (4 results) (of which Peer Reviewed: 4 results,  Open Access: 4 results) Presentation (4 results) (of which Invited: 1 results)

  • [Journal Article] Protein kinase Cα activation switches YAP1 from TEAD‐mediated signaling to p73‐mediated signaling2022

    • Author(s)
      Sinclear Caleb Kwame、Maruyama Junichi、Nagashima Shunta、Arimoto‐Matsuzaki Kyoko、Kuleape Joshua Agbemefa、Iwasa Hiroaki、Nishina Hiroshi、Hata Yutaka
    • Journal Title

      Cancer Science

      Volume: 113 Issue: 4 Pages: 1305-1320

    • DOI

      10.1111/cas.15285

    • Related Report
      2022 Annual Research Report
    • Peer Reviewed / Open Access
  • [Journal Article] DNA Damage Triggers the Nuclear Accumulation of RASSF6 Tumor Suppressor Protein via CDK9 and BAF53 To Regulate p53 Target Gene Transcription2022

    • Author(s)
      Kuleape Joshua Agbemefa、Hossain Shakhawoat、Sinclear Caleb Kwame、Shimizu Takanobu、Iwasa Hiroaki、Maruyama Junichi、Arimoto-Matsuzaki Kyoko、Nishina Hiroshi、Hata Yutaka
    • Journal Title

      Molecular and Cellular Biology

      Volume: 42 Issue: 2 Pages: 310-321

    • DOI

      10.1128/mcb.00310-21

    • Related Report
      2021 Research-status Report
    • Peer Reviewed / Open Access
  • [Journal Article] Characterization of mouse embryonic fibroblasts derived from <i>Rassf6</i> knockout mice shows the implication of Rassf6 in the regulation of NF‐κB signaling2021

    • Author(s)
      Morishita Mayu、Arimoto‐Matsuzaki Kyoko、Kitamura Masami、Niimura Kyohei、Iwasa Hiroaki、Maruyama Junichi、Hiraoka Yuichi、Yamamoto Kohei、Kitagawa Masanobu、Miyamura Norio、Nishina Hiroshi、Hata Yutaka
    • Journal Title

      Genes to Cells

      Volume: 26 Issue: 12 Pages: 999-1013

    • DOI

      10.1111/gtc.12901

    • Related Report
      2021 Research-status Report
    • Peer Reviewed / Open Access
  • [Journal Article] CSE1L promotes nuclear accumulation of transcriptional coactivator TAZ and enhances invasiveness of human cancer cells.2021

    • Author(s)
      Nagashima S, Maruyama J, Honda K, Kondoh Y, Osada H, Nawa M, Nakahama KI, Ishigami-Yuasa M, Kagechika H, Sugimura H, Iwasa H, Arimoto-Matsuzaki K, Nishina H, Hata Y
    • Journal Title

      Journal of Biological Chemistry

      Volume: 297 Issue: 1 Pages: 100803-100803

    • DOI

      10.1016/j.jbc.2021.100803

    • Related Report
      2021 Research-status Report
    • Peer Reviewed / Open Access
  • [Presentation] Rassf6欠損マウスにおいて腫瘍抑制分子Rassf6はNF-κBシグナルの制御に関与する2022

    • Author(s)
      森下 真由, 松崎 京子, 北村 雅美, 新村 恭平, 岩佐 宏晃, 丸山 順一, 平岡 優一, 山本 浩平, 北川 昌伸, 宮村 憲央, 仁科 博史
    • Organizer
      第95回 日本生化学会年会
    • Related Report
      2022 Annual Research Report
  • [Presentation] 早老症モデルマウスを用いた骨格筋幹細胞の加齢性変化の解析2021

    • Author(s)
      松崎 京子, Lu Dai, 新村 恭平, 森元 悠矢, 平岡 優一, 山本 浩平, 畑 裕
    • Organizer
      第94回 日本生化学大会
    • Related Report
      2021 Research-status Report
    • Invited
  • [Presentation] Analysis of satellite cells using aging model mice2020

    • Author(s)
      松崎京子
    • Organizer
      第43回 日本分子生物学会年会
    • Related Report
      2020 Research-status Report
  • [Presentation] Characterization of Hutchinson-Gilford Progeria Syndrome mouse as a model to study sarcopenia.2019

    • Author(s)
      Lu DAI, Kyoko ARIMOTO-MATSUZAKI, Kohei YAMAMOTO, Yuichi HIRAOKA, Yutaka HATA
    • Organizer
      第92回日本生化学会大会
    • Related Report
      2019 Research-status Report

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Published: 2019-04-18   Modified: 2024-01-30  

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