Epidermal growth factor and the regulation of amnion prostaglandin biosynthesis

Prostaglandins Leukot Essent Fatty Acids. 1991 Sep;44(1):57-9. doi: 10.1016/0952-3278(91)90145-u.

Abstract

The production of prostaglandins by amnion is a key factor in the mechanism of human parturition yet the regulation of prostaglandin biosynthesis in amnion is poorly understood. Hence, we have investigated the regulation of epidermal growth factor (EGF) stimulation of prostaglandin biosynthesis in human amnion cells. This stimulatory action is inhibited by cycloheximide or actinomycin D at high concentrations, but enhanced at much lower concentrations of these protein synthesis inhibitors. An amnion-produced prostaglandin inhibitor or immediate early gene action may explain these effects. Pretreatment with phorbol esters (inhibition of protein kinase C activity) reduces basal prostaglandin production and attenuates the stimulatory action of EGF on prostaglandin biosynthesis. Hence, amnion prostaglandin biosynthesis is dependent partly on protein kinase C activity.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amnion / drug effects
  • Amnion / metabolism*
  • Cells, Cultured
  • Dinoprostone / biosynthesis
  • Epidermal Growth Factor / pharmacology*
  • Humans
  • Phorbol Esters / pharmacology
  • Prostaglandins / biosynthesis*

Substances

  • Phorbol Esters
  • Prostaglandins
  • Epidermal Growth Factor
  • Dinoprostone