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

J Biol Chem. 2011 Nov 4;286(44):38456-38465. doi: 10.1074/jbc.M111.271270. Epub 2011 Sep 18.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 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
  • Muscular Atrophy / metabolism*
  • Protein Biosynthesis*
  • Transfection


  • MicroRNAs
  • Mirn23b microRNA, mouse