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 17β-estradiol (E2). It has been convincingly shown that E2 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 E2 action at the cell membrane and discrete biological actions in the cell has been strengthened. There is now convincing in vitro evidence that E2 can modulate the functions of neural and vascular cells via non-genomic actions. Thus, the actions of discrete pools of E2 receptors are likely to contribute to the overall effects of the sex steroids.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism