STAT5A promotes adipogenesis in nonprecursor cells and associates with the glucocorticoid receptor during adipocyte differentiation.

Abstract

The differentiation of adipocytes is regulated by the activity of a variety of transcription factors, including peroxidase proliferator-activated receptor (PPAR)-gamma and C/EBPalpha. Our current study demonstrates that ectopic expression of STAT5A, such as that of PPAR-gamma and C/EBPalpha, promotes adipogenesis in two nonprecursor fibroblast cell lines. Using morphologic and biochemical criteria, we have demonstrated that STAT5A and the combination of STAT5A and STAT5B are sufficient to induce the expression of early and late adipogenic markers in BALB/c and NIH-3T3 cells. Yet, the ectopic expression of STAT5B alone does not induce the expression of adipocyte genes, but enhances the induction of these genes in cells also expressing STAT5A. This finding suggests that STAT5A and STAT5B do not function identically in adipocytes. In addition, these studies demonstrate that the phosphorylation of STAT5 proteins may play a role in adipogenesis. Moreover, we have shown that STAT5A is associated with the glucocorticoid receptor during adipogenesis in a highly regulated manner.