Abstract |
Muscle atrophy is caused by accelerated protein degradation and occurs in many pathological states. Two muscle-specific ubiquitin ligases, MAFbx/atrogin-1 and muscle RING-finger 1 (MuRF1), are prominently induced during muscle atrophy and mediate atrophy-associated protein degradation. Blocking the expression of these two ubiquitin ligases provides protection against muscle atrophy. Here we report that miR-23a suppresses the translation of both MAFbx/atrogin-1 and MuRF1 in a 3'-UTR-dependent manner. Ectopic expression of miR-23a is sufficient to protect muscles from atrophy in vitro and in vivo. Furthermore, miR-23a transgenic mice showed resistance against glucocorticoid-induced skeletal muscle atrophy. These data suggest that suppression of multiple regulators by a single miRNA can have significant consequences in adult tissues.
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Authors | Shogo Wada, Yoshio Kato, Mitsuharu Okutsu, Shigeru Miyaki, Katsuhiko Suzuki, Zhen Yan, Stefano Schiaffino, Hiroshi Asahara, Takashi Ushida, Takayuki Akimoto |
Journal | The Journal of biological chemistry
(J Biol Chem)
Vol. 286
Issue 44
Pg. 38456-38465
(Nov 04 2011)
ISSN: 1083-351X [Electronic] United States |
PMID | 21926429
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- MicroRNAs
- Mirn23b microRNA, mouse
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Topics |
- Animals
- Base Sequence
- Cell Line
- Gene Expression Regulation
- Male
- Mice
- Mice, Inbred C57BL
- Mice, Transgenic
- MicroRNAs
(metabolism)
- Molecular Sequence Data
- Muscle, Skeletal
(metabolism)
- Muscular Atrophy
(genetics, metabolism)
- Protein Biosynthesis
- Transfection
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