Citation

  • Authors: Chen, J. G., Li, X., Huang, H. Y., Liu, H. L., Liu, D. G., Song, T. J., Ma, C. G., Ma, D., Song, H. Y., Tang, Q. Q.
  • Year: 2006
  • Journal: Biochem Biophys Res Commun 347 821-6
  • Applications: in vitro / DNA / jetPEI
  • Cell type: 3T3-L1
    Description: Murine embryonic fibroblasts
    Known as: NIH/3T3-L1, NIH-3T3-L1

Abstract

PAI-1 is expressed and secreted by adipose tissue which may mediate the pathogenesis of obesity-associated cardiovascular complications. Evidence is presented in this report that PAI-1 is not expressed by preadipocyte, but significantly induced during 3T3-L1 adipocyte differentiation and the PAI-1 expression correlates with the induction of peroxisome proliferator-activated receptor gamma (PPARgamma). A peroxisome proliferator responsive element (PPRE)-like cis-element (-206TCCCCCATGCCCT-194) is identified in the mouse PAI-1 gene promoter by electrophoretic mobility shift assay (EMSA) combined with transient transfection experiments; the PPRE-like cis-element forms a specific DNA-protein complex only with adipocyte nuclear extracts, not with preadipocyte nuclear extracts; the DNA-protein complex can be totally competed away by non-labeled consensus PPRE, and can be supershifted with PPARgamma antibody. Mutation of this PPRE-like cis-element can abolish the transactivation of mouse PAI-1 promoter mediated by PPARgamma. Specific PPARgamma ligand Pioglitazone can significantly induce the PAI-1 expression, and stimulate the secretion of PAI-1 into medium.

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