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Extrinsic mechanical stress involves in inhibitory effect of muscle atrophy

Research Project

Project/Area Number 16K01856
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Applied health science
Research InstitutionNadogaya Hospital (Laboratory for Mechanical Medicine, Nadogaya Research Institute)

Principal Investigator

Ichiro Harada  社会医療法人社団蛍水会名戸ヶ谷病院(名戸ヶ谷研究所メカノメディスン部門), メカノメディスン部門, 主任研究員 (00361759)

Project Period (FY) 2016-04-01 – 2019-03-31
Project Status Completed (Fiscal Year 2018)
Budget Amount *help
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Keywords筋萎縮 / 細胞外マトリクス / 線維芽細胞 / メカノトランスダクション / メカニカルストレス / 骨格筋 / 組織硬化 / 不動化モデル / 硬化組織
Outline of Final Research Achievements

It is well known that mechanical stimulation through a physical activity contribute for homeostasis of organs. However, how such mechanical stimuli affect organs and tissue is largely unidentified in cellular and molecular level. Especially for musculotendinous tissue homeostasis, it is recognized that importance of mechanical stimuli is not only through a physical activity but also through extrinsic stimuli, such as massage or physical stretch. Here, we studied how extrinsic mechanical stimuli inhibit muscle atrophy or fibrosis, using mice and cultured cells. As the results, we found that there are several fibroblasts exhibit different phenotype, and fibroblasts, which actively divide on stiffer scaffold, involved in muscle differentiation and maintenance.

Academic Significance and Societal Importance of the Research Achievements

これまでに、筋組織には造血細胞由来ではない複数種の単核細胞が存在することが示唆されていたが、それはすべて同一の前駆細胞由来であることが示されていた。その細胞は異所性の脂肪となることも分かっているが、線維芽細胞へ分化した後の運命についてはまだ未解明であった。本研究で示された数種類の線維芽細胞も同一の系譜であることは確認されているが、線維芽細胞化の後にことなる表現系となっていることは新しい発見である。また、組織の硬さに応答して増殖し筋組織の恒常性維持に関わっていることは、今後加齢に伴う筋萎縮に対して新しい予防方法考案に大いに貢献する。

Report

(4 results)
  • 2018 Annual Research Report   Final Research Report ( PDF )
  • 2017 Research-status Report
  • 2016 Research-status Report
  • Research Products

    (2 results)

All 2018 2016

All Journal Article (1 results) (of which Int'l Joint Research: 1 results,  Peer Reviewed: 1 results,  Open Access: 1 results) Presentation (1 results)

  • [Journal Article] MEKK1-dependent phosphorylation of calponin-3 tunes cell contractility2016

    • Author(s)
      Hirata H, Ku WC, Yip AK, Ursekar CP, Kawauchi K, Roy A, Guo AK, Vedula SR, Harada I, Chiam KH, Ishihama Y, Lim CT, Sawada Y, Sokabe M
    • Journal Title

      J Cell Sci

      Volume: 129(19) Issue: 19 Pages: 3574-3582

    • DOI

      10.1242/jcs.189415

    • Related Report
      2016 Research-status Report
    • Peer Reviewed / Open Access / Int'l Joint Research
  • [Presentation] 上皮増殖因子の局所刺激に応答した細胞の走化性の解析2018

    • Author(s)
      須山孟、荒津史裕、原田伊知郎
    • Organizer
      第41回日本分子生物学会年会
    • Related Report
      2018 Annual Research Report

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Published: 2016-04-21   Modified: 2020-03-30  

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