Phorbol 12-myristate 13-acetate inhibition of leukotriene D4-induced signal transduction was rapidly reversed by staurosporine

Biochem Biophys Res Commun. 1988 Dec 15;157(2):521-9. doi: 10.1016/s0006-291x(88)80280-8.

Abstract

Activation of leukotriene D4 receptors results in phospholipase C-mediated breakdown of phosphatidylinositol and increases in intracellular Ca2+ in U-937 cells. Treatment (10 min) with phorbol 12-myristate 13-acetate blocked leukotriene D4-induced phosphatidylinositol metabolism and Ca2+ mobilization (IC50 = 0.2 nM). Treatment with 10 nM phorbol 12-myristate 13-acetate produced blockade which was complete within 1 min and no recovery was observed over 7 days. Addition of the protein kinase C inhibitor staurosporine (100 nM) to U-937 cells pretreated with phorbol 12-myristate 13-acetate for 5 min or 24 hr resulted in a rapid reappearance of leukotriene D4-induced Ca2+ mobilization. Half of the response recovered within 2 min, with complete recovery in 20 min. Staurosporine produced a concentration-related recovery of signal transduction, with an EC50 of 30 nM. These data describe cells which have a novel response to phorbol 12-myristate 13-acetate in that the inhibition of leukotriene D4 signal transduction is persistent and yet rapidly reversed by staurosporine.

MeSH terms

  • Alkaloids / pharmacology*
  • Calcium / metabolism
  • Humans
  • In Vitro Techniques
  • Inositol Phosphates / metabolism
  • Phosphatidylinositols / metabolism
  • Protein Kinase C / antagonists & inhibitors*
  • SRS-A / pharmacology*
  • Staurosporine
  • Tetradecanoylphorbol Acetate / pharmacology*
  • Time Factors
  • Tumor Cells, Cultured

Substances

  • Alkaloids
  • Inositol Phosphates
  • Phosphatidylinositols
  • SRS-A
  • Protein Kinase C
  • Staurosporine
  • Tetradecanoylphorbol Acetate
  • Calcium