Premium
Translational Supression of Atrogin‐1 and MuRF1 by miR‐23a Integrates Resistance to Skeletal Muscle Atrophy
Author(s) -
Wada Shogo,
Kato Yoshio,
Ushida Takashi,
Akimoto Takayuki
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1086.3
Subject(s) - atrophy , ubiquitin , muscle atrophy , ectopic expression , protein degradation , in vivo , skeletal muscle , atg12 , autophagy , microbiology and biotechnology , biology , chemistry , translation (biology) , medicine , endocrinology , messenger rna , biochemistry , apoptosis , gene , genetics , atg5
Muscle atrophy is caused by accelerated protein degradation and occurs in many pathological states. Two muscle‐specific ubiquitin ligases, atrogin‐1/MAFbx 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.