Poly ADP ribose-polymerase inhibitors prevent the upregulation of ICAM-1 and E-selectin in response to Th1 cytokine stimulation

Inflammation. 2001 Jun;25(3):157-63. doi: 10.1023/a:1011032313445.

Abstract

We studied the role of poly-ADP-ribose polymerase (PARP) in the mobilization of ICAM-1, VCAM-1, and E-selectin by TNF-alpha and IL-1beta in cultured human endothelial cells. Enzyme linked immunosorbent analysis (ELISA) was used to assess if ICAM-1, VCAM-1, and E-selectin were expressed at the cell surface, and if PARP inhibition (using the selective PARP inhibitor GPI 6150) blocked the induced expression. Endothelial cell adhesion molecule expression was evaluated at 4 and at 24 h after cytokine stimulation. At 4 h ICAM-1 and E-selectin, but not VACM-1, were stimulated by both IL-1beta and TNF-alpha. Blocking PARP via GPI 6150 only affected TNF-alpha induced E-selectin expression at 4 hours. ICAM-1, VCAM-1, and E-selectin expression were all stimulated by both IL-1beta and TNF-alpha in the 24 h assays. PARP inhibition with GPI 6150 blocked the IL-1beta mediated stimulation of both ICAM-1 and E-selectin expression, and blocked TNF-alpha stimulation of ICAM-1 expression at 24 h. These experiments suggest that specific PARP inhibition may provide a novel method of controlling leukocyte dependent inflammation through the reduction of ICAM-1 and E-selectin expression in endothelial cells in response to cytokines.

MeSH terms

  • Benzopyrans / pharmacology
  • Cell Adhesion / drug effects
  • Cell Adhesion / immunology
  • Cells, Cultured
  • Cytokines / pharmacology*
  • E-Selectin / metabolism*
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / immunology
  • Enzyme Inhibitors / pharmacology
  • Humans
  • Inflammation / etiology
  • Inflammation / prevention & control
  • Intercellular Adhesion Molecule-1 / metabolism*
  • Interleukin-1 / pharmacology
  • Isoquinolines / pharmacology
  • Leukocytes / drug effects
  • Leukocytes / immunology
  • Poly(ADP-ribose) Polymerase Inhibitors*
  • Th1 Cells / immunology*
  • Tumor Necrosis Factor-alpha / pharmacology
  • Up-Regulation / drug effects
  • Vascular Cell Adhesion Molecule-1 / metabolism

Substances

  • Benzopyrans
  • Cytokines
  • E-Selectin
  • Enzyme Inhibitors
  • GPI 6150
  • Interleukin-1
  • Isoquinolines
  • Poly(ADP-ribose) Polymerase Inhibitors
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1