Interleukin-4 mediates STAT6 activation in 3T3-L1 preadipocytes but not adipocytes

Biochem Biophys Res Commun. 2000 Jan 19;267(2):516-20. doi: 10.1006/bbrc.1999.1993.

Abstract

STAT6 is abundantly expressed in 3T3-L1 preadipocytes and adipocytes but activating ligands are not well defined. In this report, we provide evidence that interleukin 4 (IL-4) induced JAK2-mediated STAT6 tyrosine phosphorylation and DNA binding in 3T3-L1 preadipocytes but not in 3T3-L1 adipocytes. Loss of IL-4-mediated STAT6 tyrosine phosphorylation occurred 2 days after preadipocytes were induced to differentiate into adipocytes but when cells remained phenotypically preadipocytes. 3T3-L1 adipocytes were still responsive to IL-4 through tyrosine phosphorylation of other cellular proteins. We conclude that IL-4 signals through STAT6 in 3T3-L1 preadipocytes but not in 3T3-L1 adipocytes. This differentiation-dependent loss of STAT6 activation may be critical for distinct biological effects of IL-4 in 3T3-L1 preadipocytes and adipocytes.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 3T3 Cells
  • Adipocytes / cytology
  • Adipocytes / drug effects*
  • Adipocytes / metabolism*
  • Animals
  • Cell Differentiation
  • Interleukin-4 / pharmacology*
  • Janus Kinase 2
  • Mice
  • Phosphorylation
  • Protein-Tyrosine Kinases / metabolism
  • Proto-Oncogene Proteins*
  • STAT6 Transcription Factor
  • Signal Transduction
  • Trans-Activators / metabolism*
  • Tyrosine / metabolism

Substances

  • Proto-Oncogene Proteins
  • STAT6 Transcription Factor
  • Stat6 protein, mouse
  • Trans-Activators
  • Interleukin-4
  • Tyrosine
  • Protein-Tyrosine Kinases
  • Jak2 protein, mouse
  • Janus Kinase 2