| Project/Area Number |
26861204
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
Nakagawa Shuji 京都府立医科大学, 医学(系)研究科(研究院), 講師 (30643382)
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| Research Collaborator |
MORIHARA TORU 京都府立医科大学, 医学研究科, 准教授 (90336735)
INOUE HIROAKI 京都府立医科大学, 医学研究科, 講師 (60457968)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 筋損傷 / HSP47 / 線維化疾患 / 筋線維芽細胞 / 線維芽細胞 / siRNA |
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| Outline of Final Research Achievements |
Damaged myofibers are susceptible to re-tearing due to scar healing by fibrosis. Heat shock protein 47 (HSP47) is a molecular chaperone that specifically acts on collagen biosynthesis. The purpose of this study was to analyze the expression of HSP 47 using muscle injury animal model and myoblast fibrosis model. We dissected the medial gastrocnemius muscle of Wistar rats and evaluated this site histologically where the expression of HSP 47 increased. TGF-β1 increased the gene expression of HSP47, COL1A1, COL3A1 on the rat myoblast cell line. Thus, HSP47 could be a therapeutic target that inhibits scar healing in muscle injury.
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