Myostatin induces autophagy in skeletal muscle in vitro

Biochem Biophys Res Commun. 2011 Dec 2;415(4):632-6. doi: 10.1016/j.bbrc.2011.10.124. Epub 2011 Nov 2.

Abstract

Myostatin is an important regulator of muscle mass that contributes to the loss of muscle mass in a number of chronic diseases. Myostatin is known to activate the expression of components of the ubiquitin-proteosomal pathway but its effect on the autophagic pathway is not known. We therefore analysed the effect of myostatin and TGF-β on autophagy in C2C12 cells by determining the effect of these proteins on LC3 processing, autophagosome formation and autophagy gene expression. Both myostatin and TGF-β increased LC3II expression and turnover as well as autophagosome formation (marked by the formation of puncta in LC3-GFP transfected cells). Myostatin also significantly increased the expression of ATG-4B and ULK-2 mRNA while TGF-β caused a trend towards an increase in these genes. We conclude that myostatin and TGF-β increase autophagy in skeletal muscle cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autophagy / drug effects
  • Autophagy / genetics
  • Autophagy / physiology*
  • Cell Line
  • Gene Expression / drug effects
  • Mice
  • Microtubule-Associated Proteins
  • Muscle, Skeletal / cytology*
  • Muscle, Skeletal / drug effects
  • Myostatin / pharmacology
  • Myostatin / physiology*
  • Protein Serine-Threonine Kinases / genetics
  • Transforming Growth Factor beta / pharmacology

Substances

  • Map1lc3b protein, mouse
  • Microtubule-Associated Proteins
  • Myostatin
  • Transforming Growth Factor beta
  • Ulk2 protein, mouse
  • Protein Serine-Threonine Kinases