Identification of factor promoting MuSC expansion like a resistance training

2021 Fiscal Year Final Research Report

• Project/Area Number: 20K21757
• Research Category: Grant-in-Aid for Challenging Research (Exploratory)
• Allocation Type: Multi-year Fund
• Review Section: Medium-sized Section 59:Sports sciences, physical education, health sciences, and related fields
• Research Institution: Osaka University
• Principal Investigator: FUKADA So-ichiro 大阪大学, 薬学研究科, 准教授 (20432445)
• Project Period (FY): 2020-07-30 – 2022-03-31
• Keywords: カルシトニン受容体 / 静止期 / 自発運動 / gp130 / Thrombospondin-1

Outline of Final Research Achievements

In this application, the mechanism of exercise-dependent proliferation of MuSCs in unloaded muscle observed in CalcR-mutant mice was found to be a disruption of the CalcR-PKA-Yap1 pathway. Thrombospondin-1, which increases in a resistance training-dependent manner, is not detectable in blood, suggesting that another factor may be responsible for the phenotypes of CalcR-mutant mice. Conversely, IL-6, a typical resistance training-dependent factor, may not be as important for MuSC proliferation in the resistance model.

Free Research Field

筋生物学

Academic Significance and Societal Importance of the Research Achievements

MuSCは骨格筋にかかる負荷の違いにより静止期と活動期を行き来する。その根底のメカニズムは，申請者が追究してきたCalcR-PKA-Yap1経路と運動依存的に血液中で増加する因子または，局所で発現するThrombospondin-1などの因子であることが明らかとなった。局所，全身性の因子を組み合わせて効率よくMuSCを増殖させ，筋線維核を増加させることができれば，筋線維核の補充による新しい治療法につながることを提示できた。