Rapid actions of plasma membrane estrogen receptors

Trends Endocrinol Metab. May-Jun 2001;12(4):152-6. doi: 10.1016/s1043-2760(01)00377-0.

Abstract

Functional evidence for the existence of plasma membrane estrogen receptors in a variety of cell types continues to accumulate. Many of these functions originate from rapid signaling events, transduced in response to 17beta-estradiol (E(2)). It has been convincingly shown that E(2) activates phosphoinositol 3-kinase and protein kinase B/AKT, and stimulates ERK and p38 MAP kinases. In part, this stems from G-protein activation and the resulting calcium flux. As a result, the link between E(2) action at the cell membrane and discrete biological actions in the cell has been strengthened. There is now convincing in vitro evidence that E(2) can modulate the functions of neural and vascular cells via non-genomic actions. Thus, the actions of discrete pools of E(2) receptors are likely to contribute to the overall effects of the sex steroids.

Publication types

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

MeSH terms

  • Animals
  • Calcium / metabolism
  • Cell Membrane / chemistry*
  • Estradiol / pharmacology
  • Humans
  • Ion Channels / drug effects
  • Ion Channels / physiology
  • Receptors, Estrogen / analysis
  • Receptors, Estrogen / drug effects
  • Receptors, Estrogen / physiology*
  • Signal Transduction

Substances

  • Ion Channels
  • Receptors, Estrogen
  • Estradiol
  • Calcium