Project/Area Number |
23790347
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
General medical chemistry
|
Research Institution | Fujita Health University |
Principal Investigator |
HITACHI Keisuke 藤田保健衛生大学, 総合医科学研究所, 助教 (10508469)
|
Project Period (FY) |
2011 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 細胞医科学 / microRNA / マイオスタチン / 骨格筋 |
Research Abstract |
Myostatin is a negative regulator of skeletal muscle mass. We previously identifiedseveral microRNAs differentially expressed in skeletal muscle of myostatin knockout mice.However, the role of the microRNAs in the regulation of skeletal muscle mass remainsunknown. In this study, we analyzed the function of microRNA in myostatin-deficient musclehypertrophy. We especially focused on miR-486, since miR-486 is reported to be a positiveregulator of IGF1/Akt signaling in skeletal muscle. We showed that canonical myostatinsignaling negatively regulates miR-486 expression at the transcriptional level.Furthermore, gain and loss of function of miR-486 demonstrated the involvement of miR-486in the regulation of C2C12 myotube size. Our results suggest that miR-486 is a potent intermediary molecule that connects myostatin and IGF1/Akt signaling in the regulation of skeletal muscle mass.
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