| Project/Area Number |
26462836
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathobiological dentistry/Dental radiology
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| Research Institution | Osaka University |
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Principal Investigator |
MAEDA Takashi 大阪大学, 歯学研究科, 准教授 (80324789)
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| Co-Investigator(Kenkyū-buntansha) |
古川 惣平 大阪大学, 歯学研究科, 教授 (80173524)
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| Co-Investigator(Renkei-kenkyūsha) |
SATO Sunao 大阪大学, 大学院歯学研究科, 講師 (70335660)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 発生・分化 / Cartducin / 骨格筋 / 筋芽細胞 / CTRP3 / C2C12細胞 / 3T3-L1細胞 / ３T３－L１細胞 / ERK1/2 / 筋分化 |
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| Outline of Final Research Achievements |
Cartducin is a member of the C1q and tumor necrosis factor-related protein (CTRP) superfamily. In the present study, we provide evidence for a physiological role of the cartducin in myogenesis using C2C12 myoblasts. Cartducin was expressed in developing skeletal muscle tissues, and the expression level of cartducin was increased during myogenic differentiation of C2C12 cells. Recombinant cartducin promoted the proliferation of undifferentiated C2C12 myoblasts and this response required activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway. In contrary, it inhibited myogenic differentiation and fusion of C2C12 cells by suppressing the expression of myogenic marker genes. Cartducin mRNA expression was increased in C2C12 myoblasts treated with TGF-β3, suggesting that TGF-β3 is one of the extracellular factors regulating cartducin expression during myogenesis. These results indicate a novel physiological role for cartducin during skeletal myogenesis.
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