期刊
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
卷 90, 期 -, 页码 145-154出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.biocel.2017.07.020
关键词
Atrophy; miR-18a; Myotubes; Igf1
资金
- National Basic Research Program of China [2015CB943103]
- Modern Agro-industry Technology Research Systems of China [CARS-37]
- National Transgenic Breeding Project of China [2014ZX08010004]
- National 863 Project of the China Ministry of Science and Technology [2012AA020601]
Muscle atrophy occurs when there is a net loss of muscle mass, leading to a change in the balance between protein synthesis and protein degradation. Igf1 is important for protein synthesis in muscle cells and can induce local skeletal muscle hypertrophy and attenuate age-related skeletal muscle atrophy via the PI3K/Akt pathway in mice, consequently restoring and improving muscle mass and strength. In this study, we show that miR-18a expression is down-regulated during C2C12 myoblast differentiation and mouse tibialis anterior muscle postnatal development. Functional studies show that forced expression of miR-18a induces myotubes atrophy and increases the expression of MuRF1, Atrogin-1 and CTSL. miR-18a also decreases the phosphorylation of both Akt and FoxO3, and an inhibitor of the PI3K/Akt pathway blocks the function of miR-18a. An analysis of miR-18a targets reveals that Igf1 is regulated by miR-18a. miR-18a suppresses the expression of Igf1 in a 3'UTR-dependent manner. These findings strongly support the idea that miR-18a has a functional role in muscle physiology and suggest that miR-18a is a potential novel therapeutic target for skeletal muscle atrophy.
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