Tumor necrosis factor-alpha inhibits peroxisome proliferator-activated receptor gamma activity at a posttranslational level in hepatic stellate cells

Am J Physiol Gastrointest Liver Physiol. 2004 May;286(5):G722-9. doi: 10.1152/ajpgi.00411.2003. Epub 2003 Dec 4.

Abstract

Diminished activity of peroxisome proliferator-activated receptor gamma (PPARgamma) is implicated in activation of hepatic stellate cells (HSC), a critical event in the development of liver fibrosis. In the present study, we investigated PPARgamma regulation by TNF-alpha in an HSC line designated as BSC. In BSC, TNF-alpha decreased both basal and ligand (GW1929)-induced PPARgamma mRNA levels without changing its protein expression. Nuclear extracts from BSC treated with TNF-alpha showed decreased binding of PPARgamma to PPAR-responsive element (PPRE) as determined by electrophoretic mobility shift assay. In BSC transiently transfected with a PPARgamma1 expression vector and a PPRE-luciferase reporter gene, TNF-alpha decreased both basal and GW1929-induced transactivation of the PPRE promoter. TNF-alpha increased activation of ERK1/2 and JNK, previously implicated in phosphorylation of Ser(82) of PPARgamma1 and resultant negative regulation of PPARgamma transactivity. In fact, TNF-alpha failed to inhibit transactivity of a Ser(82)Ala PPARgamma1 mutant in BSC. TNF-alpha-mediated inhibition of PPARgamma transactivity was not blocked with a Ser(32)Ala/Ser(36)Ala mutant of inhibitory NF-kappaBalpha (IkappaBalpha). These results suggest that TNF-alpha inhibits PPARgamma transactivity in cultured HSC, at least in part, by diminished PPARgamma-PPRE (DNA) binding and ERK1/2-mediated phosphorylation of Ser(82) of PPARgamma1, but not via the NF-kappaB pathway.

Publication types

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

MeSH terms

  • Animals
  • Benzophenones / pharmacology
  • Cell Line
  • DNA / metabolism
  • Enzyme Activation
  • JNK Mitogen-Activated Protein Kinases
  • Liver / metabolism*
  • Male
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases / metabolism
  • Mutation
  • NF-kappa B / metabolism
  • Phosphorylation / drug effects
  • Protein Processing, Post-Translational / drug effects*
  • RNA, Messenger / antagonists & inhibitors
  • Rats
  • Rats, Wistar
  • Receptors, Cytoplasmic and Nuclear / antagonists & inhibitors*
  • Receptors, Cytoplasmic and Nuclear / genetics*
  • Response Elements
  • Transcription Factors / antagonists & inhibitors*
  • Transcription Factors / genetics*
  • Transcription, Genetic / drug effects
  • Transcriptional Activation / drug effects
  • Tumor Necrosis Factor-alpha / pharmacology*
  • Tyrosine / analogs & derivatives*
  • Tyrosine / pharmacology

Substances

  • Benzophenones
  • NF-kappa B
  • RNA, Messenger
  • Receptors, Cytoplasmic and Nuclear
  • Transcription Factors
  • Tumor Necrosis Factor-alpha
  • Tyrosine
  • DNA
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases
  • GW 1929