Transforming growth factor beta 2 differentially modulates interleukin-1 beta- and tumour-necrosis-factor-alpha-stimulated phospholipase A2 and prostaglandin E2 synthesis in rat renal mesangial cells

Biochem J. 1990 Aug 15;270(1):269-71. doi: 10.1042/bj2700269.

Abstract

Treatment of rat glomerular mesangial cells with transforming growth factor beta 2 (TGF beta 2) stimulates prostaglandin E2 (PGE2) synthesis. Actinomycin D, cycloheximide and diclofenac attenuate the TGF beta 2-induced PGE2 formation. As shown previously, two proinflammatory cytokines, interleukin 1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF alpha), are potent stimuli for PGE2 and phospholipase A2 secretion from mesangial cells. We report here that, whereas TGF beta 2 potentiates the IL-1 beta- and TNF alpha-evoked PGE2 production, it strongly inhibits the phospholipase A2 secretion induced by both cytokines. In addition, the inhibitory effect of TGF beta 2 on phospholipase A2 secretion is not due to the augmented PGE2 formation.

MeSH terms

  • Animals
  • Cells, Cultured
  • Dinoprostone / biosynthesis*
  • Dose-Response Relationship, Drug
  • Glomerular Mesangium / metabolism*
  • In Vitro Techniques
  • Interleukin-1 / pharmacology*
  • Phospholipases / metabolism*
  • Phospholipases A / metabolism*
  • Phospholipases A2
  • Rats
  • Time Factors
  • Transforming Growth Factors / pharmacology*
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Interleukin-1
  • Tumor Necrosis Factor-alpha
  • Transforming Growth Factors
  • Phospholipases
  • Phospholipases A
  • Phospholipases A2
  • Dinoprostone