Project/Area Number |
15K08229
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General pharmacology
|
Research Institution | Tottori University (2016-2017) Shiga University of Medical Science (2015) |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
森野 勝太郎 滋賀医科大学, 医学部, 助教 (90444447)
|
Co-Investigator(Renkei-kenkyūsha) |
SAKURAI Hidetoshi 京都大学, iPS細胞研究所, 准教授 (80528745)
TAWA Masashi 滋賀医科大学, 医学部, 助教 (10510274)
|
Research Collaborator |
IWASAKI Hirotaka
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | 骨格筋細胞 / 脂肪酸受容体 / 血管内皮細胞 / インスリン抵抗性 / 幹細胞機能 |
Outline of Final Research Achievements |
In this study, we have established human induced-pluripotent stem (hiPS) cells transfected with MyoD expression vector, which differentiate to myotubes with more than 80% efficiencies (MyoD-hiPS cells). Using this system, we have detected a unique microRNA, miR-494 which was downregulated after myogenic induction. To explore the therapeutic potential of miR-494, we investigated the role of miR-494 during human skeletal myogenesis. In MyoD-hiPS cells transfected with miR-494 precursor, the level of type IIa myofiber marker proteins specifically decreased, while no change in the total number of cells was observed. In contrast, the expression of both type I and type IIx myofiber markers was unaffected by miR-494 overexpression. Furthermore, miR-494 overexpression suppressed mitochondrial oxygen consumption rate concomitant with the inhibition of myotube formation. These results suggest that miR-494 could be a therapeutic target for muscular diseases, such as sarcopenia.
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