Depletion of mammalian target of rapamycin (mTOR) via siRNA mediated knockdown leads to stabilization of beta-catenin and elicits distinct features of cardiomyocyte hypertrophy

FEBS Lett. 2010 Jan 4;584(1):74-80. doi: 10.1016/j.febslet.2009.10.080.

Abstract

Cardiac myocyte growth is under differential control of mammalian target of rapamycin (mTOR) and glycogen-synthase-kinase-3beta (GSK3beta). Whereas active GSK3beta negatively regulates growth and down-regulates cellular protein synthesis, activation of the mTOR pathway promotes protein expression and cell growth. Here we report that depletion of mTOR via siRNA mediated knockdown causes marked down-regulation of GSK3beta protein in cardiac myocytes. As a result, GSK3beta target protein beta-catenin becomes stabilized and translocates into the nucleus. Moreover, mTOR knockdown leads to increase in cardiac myocyte surface area and produces an up-regulation of the fetal gene program. Our findings suggest a new type of convergence of mTOR and GSK3beta activities, indicating that GSK3beta-dependent stabilization of beta-catenin in cardiac myocytes is influenced by mTOR.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cardiomegaly / genetics
  • Cardiomegaly / metabolism*
  • Cardiomegaly / pathology
  • Cells, Cultured
  • Gene Knockdown Techniques
  • Glycogen Synthase Kinase 3 / metabolism*
  • Glycogen Synthase Kinase 3 beta
  • Myocytes, Cardiac / metabolism*
  • Myocytes, Cardiac / pathology
  • Protein Kinases / genetics
  • Protein Kinases / metabolism*
  • Protein Stability
  • RNA, Small Interfering / genetics
  • Rats
  • Rats, Wistar
  • Sirolimus / pharmacology
  • TOR Serine-Threonine Kinases
  • beta Catenin / metabolism*

Substances

  • RNA, Small Interfering
  • beta Catenin
  • Protein Kinases
  • Glycogen Synthase Kinase 3 beta
  • Gsk3b protein, rat
  • TOR Serine-Threonine Kinases
  • Glycogen Synthase Kinase 3
  • Sirolimus