Molecular basis for antagonism between PDGF and the TGFbeta family of signalling pathways by control of miR-24 expression

EMBO J. 2010 Feb 3;29(3):559-73. doi: 10.1038/emboj.2009.370. Epub 2009 Dec 17.

Abstract

Modulation of the vascular smooth-muscle-cell (vSMC) phenotype from a quiescent 'contractile' phenotype to a proliferative 'synthetic' phenotype has been implicated in vascular injury repair, as well as pathogenesis of vascular proliferative diseases. Both bone morphogenetic protein (BMP) and transforming growth factor-beta (TGFbeta)-signalling pathways promote a contractile phenotype, while the platelet-derived growth factor-BB (PDGF-BB)-signalling pathway promotes a switch to the synthetic phenotype. Here we show that PDGF-BB induces microRNA-24 (miR-24), which in turn leads to downregulation of Tribbles-like protein-3 (Trb3). Repression of Trb3 coincides with reduced expression of Smad proteins and decrease in BMP and TGFbeta signalling, promoting a synthetic phenotype in vSMCs. Inhibition of miR-24 by antisense oligonuclotides abrogates the downregulation of Trb3 as well as pro-synthetic activity of the PDGF-signalling pathway. Thus, this study provides a molecular basis for the antagonism between the PDGF and TGFbeta pathways, and its effect on the control of the vSMC phenotype.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Becaplermin
  • COS Cells
  • Cells, Cultured
  • Chlorocebus aethiops
  • Drug Antagonism
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / physiology
  • Humans
  • Male
  • Mice
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • MicroRNAs / physiology
  • Mink
  • Models, Biological
  • Muscle Contraction / drug effects
  • Muscle Contraction / genetics
  • Myocytes, Smooth Muscle / drug effects
  • Myocytes, Smooth Muscle / metabolism
  • Myocytes, Smooth Muscle / physiology
  • Platelet-Derived Growth Factor / antagonists & inhibitors*
  • Platelet-Derived Growth Factor / pharmacology
  • Platelet-Derived Growth Factor / physiology
  • Protein Kinases / genetics
  • Protein Kinases / metabolism
  • Protein Serine-Threonine Kinases / antagonists & inhibitors
  • Proto-Oncogene Proteins c-sis
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction / drug effects
  • Signal Transduction / genetics
  • Transforming Growth Factor beta / antagonists & inhibitors*
  • Transforming Growth Factor beta / pharmacology
  • Transforming Growth Factor beta / physiology

Substances

  • MIRN24 microRNA, human
  • MIRN24 microRNA, rat
  • MicroRNAs
  • Platelet-Derived Growth Factor
  • Proto-Oncogene Proteins c-sis
  • Transforming Growth Factor beta
  • Trib3 protein, rat
  • Becaplermin
  • Protein Kinases
  • Protein Serine-Threonine Kinases