GPER Inhibition of Coronary Artery Smooth Muscle Cell Migration and Proliferation
MetadataShow full item record
Our research investigated a possible target for cardiovascular disease treatment via the G-protein coupled estrogen receptor (GPER). Estrogen mitigates vascular smooth muscle cell (VSMC) proliferation and migration, which plays an important role in the pathogenesis of atherosclerosis, the leading cause of heart disease. GPER has been reported to inhibit VSMC proliferation but the mechanism and pathway is still unclear. Furthermore, an effect of GPER on coronary artery smooth muscle cell (CASMC) migration is also unknown. A thorough understanding of the GPER cell signaling pathway and its effects on VSMC migration and proliferation is important for developing drug therapies for the treatment of cardiovascular diseases. We studied the signaling pathway using Western Blot analysis. Our results suggest that GPER inhibits VSMC proliferation via inhibition of the epidermal growth factor receptor (EGFR). This conclusion is based on the G-1 induced decrease in phospho-ERK ½ phosphorylation levels. We explored a potential role of GPER in inhibiting human and porcine CASMC migration, using a wound scratch assay. Our results demonstrated that after 24 hours of treatment G-1 (selective GPER agonist) inhibited both serum-and PDGF-stimulated migration of porcine CASMC. In addition, G15 (selective GPER antagonist) lessened the effect of G-1. These results display that GPER inhibits migration. These findings could be a novel, non-genomic mechanism whereby estrogen could attenuate the development of coronary atherosclerotic lesions.
SubjectG-protein coupled estrogen receptor
smooth muscle cell
Szynkarski, Claudia Kay (2013). GPER Inhibition of Coronary Artery Smooth Muscle Cell Migration and Proliferation. Honors and Undergraduate Research. Available electronically from