Tumor necrosis factor alpha and interleukin-1 beta but not interferon gamma induce vascular cell adhesion molecule-1 expression on primary cultured murine hepatocytes

Biochem Biophys Res Commun. 1995 Apr 6;209(1):335-42. doi: 10.1006/bbrc.1995.1508.

Abstract

Inflammatory cytokines such as tumor necrosis factor alpha (TNF alpha), interferon gamma (IFN gamma) and interleukin-1 beta (IL-1 beta) play important roles in the mechanisms of hepatitis. The effects of these cytokines on the expression of vascular cell adhesion molecule-1 (VCAM-1) in hepatocytes were examined. TNF alpha and IL-1 beta but not IFN gamma or IL-6 induced VCAM-1 expression on primary cultured murine hepatocytes in a dose- and a time-dependent fashion. TNF alpha is significantly more effective than IL-1 beta on the induction of VCAM-1 expression. The results of RT-PCR demonstrate that these cytokines regulate VCAM-1 expression at mRNA level. These results suggest that TNF alpha and IL-1 beta participate in the pathogenesis of hepatitis via induction of VCAM-1 molecules on hepatocytes.

MeSH terms

  • Animals
  • Base Sequence
  • Cell Adhesion Molecules / biosynthesis*
  • Cell Adhesion Molecules / genetics
  • Cells, Cultured
  • DNA Primers
  • Interferon-gamma / pharmacology*
  • Interleukin-1 / pharmacology*
  • Liver / cytology
  • Liver / metabolism*
  • Mice
  • Molecular Sequence Data
  • Polymerase Chain Reaction
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology*
  • Vascular Cell Adhesion Molecule-1

Substances

  • Cell Adhesion Molecules
  • DNA Primers
  • Interleukin-1
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • Interferon-gamma