The role of Stat and C/EBP transcription factors in the synergistic activation of rat serine protease inhibitor-3 gene by interleukin-6 and dexamethasone

Biochem J. 1996 Feb 1;313 ( Pt 3)(Pt 3):1019-27. doi: 10.1042/bj3131019.

Abstract

The rat serine proteinase inhibitor 3 gene is activated by interleukin 6 (IL-6) and glucocorticoids in hepatic cells. We report here that a 147 bp promoter is sufficient for both IL-6 stimulation and glucocorticoid enhancement of IL-6 induced transcription. Within this region we identified two functional elements binding transcription factors from the C/EBP (CCAAT/enhancer binding proteins) and Stat (signal transducers and activators of transcription) families. Mutations introduced into the Stat binding site resulted in a loss of responsiveness, showing that this element is indispensable for activation. In contrast, the promoter containing the mutated C/EBP binding site was still responsive to IL-6 and glucocorticoids; however, the magnitude of the induction was decreased by 50%. The Stat binding element is an enhancer capable of conferring both responsiveness to IL-6 and partial enhancement of glucocorticoids on to a heterologous promoter. In response to IL-6 this element rapidly binds acute-phase response factor (APRF/Stat3) and, later, the protein(s) that require ongoing protein synthesis and is recognized by anti-Stat3 antibodies. In addition, long-term treatment with IL-6 results in sustained phosphorylation of APRF /Stat3.

Publication types

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

MeSH terms

  • Acute-Phase Proteins / metabolism*
  • Animals
  • Base Sequence
  • Binding Sites / genetics
  • CCAAT-Enhancer-Binding Proteins
  • Cell Line
  • DNA Primers / genetics
  • DNA-Binding Proteins / metabolism*
  • Dexamethasone / pharmacology*
  • Enhancer Elements, Genetic
  • Gene Expression Regulation / drug effects
  • Humans
  • Interleukin-6 / pharmacology*
  • Molecular Sequence Data
  • Mutagenesis, Site-Directed
  • Nuclear Proteins / metabolism*
  • Phosphorylation
  • Point Mutation
  • Promoter Regions, Genetic
  • Rats
  • STAT3 Transcription Factor
  • Serine Proteinase Inhibitors / genetics*
  • Trans-Activators / metabolism*
  • Transcription Factors / metabolism*
  • Transfection

Substances

  • Acute-Phase Proteins
  • CCAAT-Enhancer-Binding Proteins
  • DNA Primers
  • DNA-Binding Proteins
  • Interleukin-6
  • Nuclear Proteins
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Serine Proteinase Inhibitors
  • Stat3 protein, rat
  • Trans-Activators
  • Transcription Factors
  • Dexamethasone