Role of nutrient sensor AMPK on regulation of myogenic inhibitory factor myostatin.
Project/Area Number |
22880006
|
Research Category |
Grant-in-Aid for Research Activity Start-up
|
Allocation Type | Single-year Grants |
Research Field |
Applied animal science
|
Research Institution | The University of Tokushima (2011) Tohoku University (2010) |
Principal Investigator |
MIYAKE Masato 徳島大学, 疾患ゲノム研究センター, 特任助教 (30588976)
|
Project Period (FY) |
2010 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥3,146,000 (Direct Cost: ¥2,420,000、Indirect Cost: ¥726,000)
Fiscal Year 2011: ¥1,508,000 (Direct Cost: ¥1,160,000、Indirect Cost: ¥348,000)
Fiscal Year 2010: ¥1,638,000 (Direct Cost: ¥1,260,000、Indirect Cost: ¥378,000)
|
Keywords | ウシ / 骨格筋 / マイオスタチン / AMPK / グルコース / 分化 / 筋芽細胞 / 初代培養 / シグナル伝達 / Smad / 成長 |
Research Abstract |
Primary myoblasts that can efficiently differentiate to myotube was established from bovine skeletal muscle. The myoblasts was expressed myoblast marker Myf5 during proliferation and differentiation marker myogenin during differentiation. These cells were inhibited differentiation and MSTN expression under low glucose condition, which activates AMPK. However expression of MSTN receptor was not changed. AMPK activator AICAR also inhibited differentiation and expression of MSTN in myotubes. The effect of antagonist of MSTN signaling was abolished by AICAR. These results suggest that AMPK regulates the action of MSTN.
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Report
(3 results)
Research Products
(17 results)