Interleukin 1 and tumor necrosis factor synergistically stimulate prostaglandin synthesis and phospholipase A2 release from rat renal mesangial cells

Biochem Biophys Res Commun. 1989 Mar 15;159(2):385-94. doi: 10.1016/0006-291x(89)90003-x.

Abstract

Treatment of rat glomerular mesangial cells with recombinant human interleukin 1 alpha (rIL-1 alpha), recombinant human interleukin 1 beta (rIL-1 beta) or recombinant human tumor necrosis factor (rTNF) induces prostaglandin E2 (PGE2) synthesis and the release of a phospholipase A2 (PLA2) activity. rIL-1 beta is significantly more potent than rIL-1 alpha or rTNF in stimulating PGE2 as well as PLA2 release from mesangial cells. When given together, rTNF interacts in a synergistic fashion with rIL-1 alpha and rIL-1 beta to enhance both, PGE2 synthesis and PLA2 release. The released PLA2 has a neutral pH optimum and is calcium-dependent. Pretreatment of cells with actinomycin D or cycloheximide inhibits basal and cytokine-stimulated PGE2 and PLA2 release.

MeSH terms

  • Animals
  • Cells, Cultured
  • Cycloheximide / pharmacology
  • Dactinomycin / pharmacology
  • Dinoprostone / antagonists & inhibitors
  • Dinoprostone / biosynthesis*
  • Drug Synergism
  • Glomerular Mesangium / metabolism*
  • Interleukin-1 / pharmacology*
  • Kinetics
  • Phospholipases / metabolism*
  • Phospholipases A / antagonists & inhibitors
  • Phospholipases A / metabolism*
  • Phospholipases A2
  • Rats
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Interleukin-1
  • Tumor Necrosis Factor-alpha
  • Dactinomycin
  • Cycloheximide
  • Phospholipases
  • Phospholipases A
  • Phospholipases A2
  • Dinoprostone