Inhibitory effect of 17 beta -estradiol on prostaglandin E2-induced phosphoinositide hydrolysis in osteoblast-like cells

Prostaglandins. 1992 Mar;43(3):271-80. doi: 10.1016/0090-6980(92)90095-b.

Abstract

We examined the effect of estradiol on PGE2-induced phosphoinositide hydrolysis and cAMP production in cloned osteoblast-like MC3T3-E1 cells. 17 beta -Estradiol pretreatment significantly inhibited the formation of inositol phosphates induced by 10 microM PGE2 in a dose-dependent manner between 1 pM and 10 nM. This effect of 17 beta -estradiol was dependent on the time of pretreatment and submaximum inhibition was observed at 4 h. However, 17 beta -estradiol had little effect on the formation of inositol phosphates induced by 20 mM NaF, a GTP-binding protein activator. The cAMP production induced by PGE2 was not influenced by 17 beta -estradiol. These results suggest that 17 beta -estradiol modulates the signal transduction by PGE2 and that the effect seems to be exerted between PGE2 receptor and the GTP-binding protein coupled to phospholipase C in osteoblast-like MC3T3-E1 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Cyclic AMP / biosynthesis
  • Dinoprostone / pharmacology*
  • Dose-Response Relationship, Drug
  • Estradiol / administration & dosage
  • Estradiol / pharmacology*
  • GTP-Binding Proteins / physiology
  • Hydrolysis
  • Inositol Phosphates / metabolism*
  • Mice
  • Osteoblasts / drug effects
  • Osteoblasts / metabolism*
  • Signal Transduction / drug effects
  • Sodium Fluoride / pharmacology
  • Type C Phospholipases / metabolism

Substances

  • Inositol Phosphates
  • Estradiol
  • Sodium Fluoride
  • Cyclic AMP
  • Type C Phospholipases
  • GTP-Binding Proteins
  • Dinoprostone