Role of G‐protein coupled estrogen receptor in estrogen‐mediated protection from cardiomyocyte hypertrophy (795.6)

Abstract

Independent, preceding studies have reported decreased risk and progression of cardiac disease in pre‐menopausal women as compared to men. 17‐β estradiol has been implicated as the molecular variable underlying this sex‐specific observation and is primarily thought to signal through nuclear receptor ER‐β. Our study seeks to understand the regulatory role of the extracellular G‐Protein Coupled Estrogen Receptor (GPER) in estrogen‐mediated protection from cardiac hypertrophy. Primary, neonatal cardiomyocytes were cultured in a sex‐dependent manner. Cellular response to the hypertrophic agent, phenylephrine, in the presence and absence of GPER activity, was assessed. Cell surface area reduction was observed in response to GPER activation, independent of nuclear estrogen receptor activity. Related studies have predominantly made use mixed cultures. Interestingly, sex‐specific cardiomyocyte cultures differ in cycling and ligand responses. The significance of sex‐specific cellular characteristics is currently being assessed. Differential expression levels identified specific miRNAs as downstream mediators of GPER, which are consistent with our previous sex‐specific Next Generation Sequencing data from hypertrophic and wild‐type hearts.NIH 5P20RR016481‐12, 8P20GM103436‐12, R15HL108192‐02Grant Funding Source: NIH 5P20RR016481‐12, 8P20GM103436‐12, R15HL108192‐02