Deletion of G Protein–Coupled Estrogen Receptor Increases Endothelial Vasoconstriction

Deletion of G protein-coupled estrogen receptor increases endothelial vasoconstriction.

Endogenous estrogens mediate protective effects in the cardiovascular system, affecting both endothelium-dependent and endothelium-independent mechanisms. Previous studies have suggested that nonselective estrogen receptor agonists such as endogenous estrogens inhibit endothelium-dependent vasoconstriction; however, the role of estrogen receptors in this response has not yet been clarified. Thi...

The G protein-coupled estrogen receptor 1 agonist G-1 disrupts endothelial cell microtubule structure in a receptor-independent manner

The G protein-coupled estrogen receptor GPER1, also known as GPR30, has been implicated in estrogen signalling, but the physiological importance of GPER1 is not fully understood. The GPER1 agonist G-1 has become an important tool to assess GPER1-mediated cellular effects. Here, we report that this substance, besides acting via GPER1, affects the microtubule network in endothelial cells. Treatme...

A direct and functional interaction between the trimeric G protein Go and Rab5 in G proteincoupled receptor signaling

Estrogen and G protein-coupled estrogen receptor agonist G-1 cause relaxation of human gallbladder

OBJECTIVE Estrogen interacts with a membrane receptor, G protein-coupled estrogen receptor (GPER). It was reported that 17β-estradiol was able to inhibit contraction of the human colon and cause relaxation of the guinea pig gallbladder, however, the involvement of GPER was not clarified. The aim of the present study was to investigate the effect of estrogen on human gallbladder motility and the...

Estrogen causes dynamic alterations in endothelial estrogen receptor expression.

Estrogen receptor (ER)alpha mediates many of the effects of estrogen on the vascular endothelium. The purpose of the present study was to determine whether estrogen modifies endothelial ERalpha expression. In experiments in cultured ovine endothelial cells, physiological concentrations of 17beta-estradiol (E2, 10(-10) to 10(-8) mol/L) caused an increase in ERalpha protein abundance that was evi...