Phorbol ester-induced activation of protein kinase C leads to increased formation of diacylglycerol in human neutrophils

Exp Cell Res. 1989 Mar;181(1):217-25. doi: 10.1016/0014-4827(89)90195-x.

Abstract

Human neutrophils stimulated with a phorbol ester (phorbol 12-myristrate 13-acetate or phorbol 12,13-dibutyrate) responded with an increase in diacylglycerol, considered the natural activator of protein kinase C. The amounts of diacylglycerol formed were considerable, reaching 700-900% of basal after 20 min. In contrast, 4-alpha-phorbol 12-myristate 13-acetate did not induce any detectable formation of diacylglycerol. Simultaneously, phorbol 12-myristate 13-acetate exposure caused increased breakdown of both phosphatidylcholine and phosphatidylinositol 4,5-bisphosphate. These results suggest that once activated, protein kinase C can positively modulate its own activity by inducing additional formation of diacylglycerol from at least two different sources.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Calcium / metabolism
  • Diglycerides / biosynthesis*
  • Enzyme Activation
  • Glycerides / biosynthesis*
  • Humans
  • Neutrophils / drug effects
  • Neutrophils / enzymology*
  • Neutrophils / metabolism
  • Phorbol 12,13-Dibutyrate / pharmacology*
  • Phosphatidylcholines / metabolism
  • Phosphatidylinositols / metabolism
  • Protein Kinase C / metabolism*
  • Tetradecanoylphorbol Acetate / pharmacology*

Substances

  • 1,2-diacylglycerol
  • Diglycerides
  • Glycerides
  • Phosphatidylcholines
  • Phosphatidylinositols
  • Phorbol 12,13-Dibutyrate
  • Protein Kinase C
  • Tetradecanoylphorbol Acetate
  • Calcium