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

Shogo Wada, Yoshio Kato, Mitsuharu Okutsu, Shigeru Miyaki, Katsuhiko Suzuki, Zhen Yan, Stefano Schiaffino, Hiroshi Asahara, Takashi Ushida, Takayuki Akimoto

Research output: Contribution to journalArticle

114 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)38456-38465
Number of pages10
JournalJournal of Biological Chemistry
Volume286
Issue number44
DOIs
Publication statusPublished - 2011 Nov 4

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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