Signal transducer and activator of transcription 5B (STAT5B) modulates adipocyte differentiation via MOF

Cell Signal. 2015 Dec;27(12):2434-43. doi: 10.1016/j.cellsig.2015.09.010. Epub 2015 Sep 22.

Abstract

The role and mechanism of signal transducer and activator of transcription 5B (STAT5B) in adipogenesis remain unclear. In this study, our data showed that Males absent on the first (MOF) protein expression was increased during 3 T3-L1 preadipocytes differentiation accompanied with STAT5B expression increasing. Over-expression STAT5B enhanced MOF promoter trans-activation in HeLa cells. Mutagenesis assay and ChIP analysis exhibited that STAT5B was able to bind MOF promoter. Knocking-down STAT5B in 3 T3-L1 preadipocytes led to decreased expression of MOF, but resulted in increased expression of peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer-binding protein α (C/EBPα) and fatty acid-binding protein 4 (Fabp4), which were important factors or enzymes for adipogenesis. We also found that knocking-down MOF in 3 T3-L1 preadipocytes resulted in increased expression of PPARγ, C/EBPα and Fabp4, which was in the same trend as STAT5B knocking-down. Over-expression MOF resulted in reduced promoter trans-activation activity of C/EBPα. These results suggest that STAT5B and MOF work as negative regulators in adipogenesis, and STAT5B modulates preadipocytes differentiation partially by regulating MOF expression.

Keywords: Adipogenesis; C/EBPα; MOF; Obesity; STAT5B.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Adipocytes / physiology*
  • Adipogenesis*
  • Animals
  • Base Sequence
  • Diet, High-Fat / adverse effects
  • HeLa Cells
  • Histone Acetyltransferases / genetics
  • Histone Acetyltransferases / metabolism*
  • Humans
  • Intra-Abdominal Fat / pathology
  • Mice
  • Mice, Inbred C57BL
  • Obesity / etiology
  • Obesity / metabolism
  • Obesity / pathology
  • Promoter Regions, Genetic
  • Protein Binding
  • STAT5 Transcription Factor / physiology*
  • Transcription, Genetic
  • Transcriptional Activation

Substances

  • STAT5 Transcription Factor
  • Stat5b protein, mouse
  • Histone Acetyltransferases
  • Kat8 protein, mouse