Molecular and Cellular Biology · 1996 · 182 citations · 73 references
Life SciencesMolecular BiologyPharmacologyCell SignalingGene ExpressionGene RegulationAdipocyte DifferentiationAdipose TissueNuclear Receptor SignalingNuclear ReceptorsRetinoic Acid SignalingSteroid Hormone SignalingAdipogenic DifferentiationDifferentiationGene Family Functional RedundancyPreadipocyte DifferentiationProtein Expression LevelsReceptor-specific LigandsRetinoid ReceptorsRetinoid X Receptors
Retinoic acid (RA) inhibits adipocyte differentiation of 3T3-L1 preadipocytes but is effective only early in adipogenesis. RA prevented induction of the adipogenic factors PPARgamma and C/EBPalpha. Using receptor-specific ligands, we determined that the effects of RA were mediated by liganded RA receptors (RARs) rather than retinoid X receptors. Preadipocytes expressed primarily RARalpha and RARgamma; during adipocyte differentiation, RARalpha gene expression was nearly constant, whereas RARgamma1 mRNA and protein levels dramatically decreased. Ectopic expression of RARgamma1 extended the period of effectiveness of RA by 24 to 48h; RARalpha expression had a similar effect, suggesting functional redundancy of RAR subtypes. Remarkably, RA inhibited differentiation when added after PPARgamma1 and PPARgamma2 proteins had already been expressed and resulted in the loss of PPARgamma proteins from cells. By 72 to 96 h after the induction of differentiation, RA failed to prevent differentiation of even ectopic-RAR-expressing cells. Thus, the unresponsiveness of 3T3-L1 preadipocytes to RA after the induction of differentiation is initially due to the reduction in cellular RAR concentration rather than to the induction of PPARgamma. At later times cells continue along the differentiation pathway in a manner which is RA and RAR independent.
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mPPAR gamma 2: tissue-specific regulator of an adipocyte enhancer.
Peter Tontonoz, E Hu, Reed A. Graves et al. · Genes & Development · 1994 · 2.2K citations · Full text