TAZ is downregulated by dexamethasone during the differentiation of 3T3-L1 preadipocytes

Biochem Biophys Res Commun. 2012 Mar 16;419(3):573-7. doi: 10.1016/j.bbrc.2012.02.074. Epub 2012 Feb 20.

Abstract

TAZ (transcriptional co-activator with PDZ binding motif) is a transcriptional modulator of mesenchymal stem cell differentiation. We have found that TAZ was expressed in postconfluent 3T3-L1 preadipocytes and downregulated during differentiation. Downregulation of TAZ was specifically mediated by dexamethasone (DEX), one component of induction cocktails routinely used in adipocyte differentiation. DEX repressed the transcription of TAZ by direct binding of the glucocorticoid receptor (GR) to the GR binding element in its promoter. More importantly, overexpression of TAZ inhibited adipogenesis and promoted the trans-differentiation of preadipocytes into osteocytes. This establishes a new functional interaction between DEX and TAZ that contributes to the mechanism of adipogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Acyltransferases
  • Adipocytes / drug effects*
  • Adipocytes / metabolism
  • Adipogenesis / drug effects*
  • Adipogenesis / genetics
  • Animals
  • Cell Differentiation / drug effects
  • Cell Differentiation / genetics
  • Dexamethasone / pharmacology*
  • Down-Regulation
  • Mice
  • Mitosis / drug effects
  • Osteocytes / cytology
  • Transcription Factors / antagonists & inhibitors*
  • Transcription, Genetic / drug effects

Substances

  • Transcription Factors
  • Dexamethasone
  • Acyltransferases
  • tafazzin protein, mouse