| Project/Area Number |
13670030
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General anatomy (including Histology/Embryology)
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| Research Institution | Osaka University of Health and Sport Sciences |
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Principal Investigator |
KAMI Katsuya Osaka University of Health and Sport Sciences, Department of Health Science, Professor, 体育学部, 教授 (20204612)
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| Co-Investigator(Kenkyū-buntansha) |
SENBA Emiko Wakayama Medical University, Department of Anatomy & Neurobiology, Professor, 医学部, 教授 (00135691)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Skeletal muscle regeneration / cytokine / muscle satellite cell / myotube / LIF / STAT3 / proliferation / differentiation / サテライト細胞 / 運動ニューロン / in situハイブリダイゼーション / 免疫組織化学 / MyoD / PCNA / 細胞内シグナル伝達分子 / 筋前駆体細胞 / 免疫組織化学法 |
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| Research Abstract |
Although growth factors and cytokines play critical roles in skeletal muscle regeneration, intracellular signaling molecules that are activated by these factors in regenerating muscles have been not elucidated. Several lines of evidence suggest that leukemia inhibitory factor (LIF) is an important cytokine for the proliferation and survival of myoblasts in vitro and acceleration of skeletal muscle regeneration. To elucidate the role of LIF signaling in regenerative responses of skeletal muscles, we examined the spatial and temporal activation patterns of a LIF-associated signaling molecule, the signal transducer and activator of transcription 3 (STAT3) proteins in regenerating rat skeletal muscles induced by crush injury. At the early stage of regeneration, activated STAT3 proteins were first detected in c-Met-positive activated satellite cell nuclei, and then continued to be activated in proliferating myoblasts expressing both PCNA and MyoD proteins. When muscle regeneration progressed, STAT3 signaling was no longer activated in differentiated myoblasts and myotubes. In addition, activation of STAT3 was also detected in myonuclei located within intact sarcolemmas of surviving myofibers which did not show signs of necrosis. These findings suggest that activation of STAT3 signaling is an important molecular event which induces the successful regeneration of injured skeletal muscles.
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