The G Protein-Coupled Estrogen Receptor (GPER-1): A Novel Regulator in the Kidney

Abstract

Gender has a crucial influence on incidence and prognosis of chronic and acute kidney diseases since women generally have a lower morbidity and mortality compared to men.1,2
Several studies have reported the capability of estrogen to promote homeostatic and protective
effects in the kidney via a pregenomic mechanism that is mediated by G protein-coupled receptor 30 (GPR30), but not by classic Estrogen Receptors (ER), ERα or ERβ.2 GPR30 was first
cloned as an orphan receptor from a Burkitt’s lymphoma cell line3 and then confirmed in other
cell lines.4 Prior studies have demonstrated that GPR30 is a specific, high affinity, Gs
-coupled
estrogen membrane receptor activated by naturally occurring and synthetic estrogens and antiestrogens including estradiol-17β, G1, tamoxifen, ICI182,780, Genestein and Bisphenol A,
but not by cortisol, progesterone or testosterone in both mammals and fish.5-15 Thus, GPR30
was designated G protein-coupled estrogen receptor-1 (GPER-1) by the International Union of
Pharmacology in 2007