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Translational suppression of atrophic regulators by microRNA-23a integrates resistance to skeletal muscle atrophy.


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.

SUBMITTER: Wada S 

PROVIDER: S-EPMC3207415 | biostudies-literature | 2011 Nov

REPOSITORIES: biostudies-literature

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Translational suppression of atrophic regulators by microRNA-23a integrates resistance to skeletal muscle atrophy.

Wada Shogo S   Kato Yoshio Y   Okutsu Mitsuharu M   Miyaki Shigeru S   Suzuki Katsuhiko K   Yan Zhen Z   Schiaffino Stefano S   Asahara Hiroshi H   Ushida Takashi T   Akimoto Takayuki T  

The Journal of biological chemistry 20110918 44


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 man  ...[more]

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