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Activation of G‐protein‐coupled estrogen receptor induces coronary artery smooth muscle re‐differentiation and inhibits migration

Estrogen attenuates vascular smooth muscle cell (VSMC) proliferation and migration. Although activation of the G‐protein‐coupled estrogen receptor (GPER) inhibits VSMC proliferation, an effect of GPER on coronary artery smooth muscle cell re‐differentiation and migration is unknown. We investigated a potential role of GPER in mediating human and porcine coronary artery SMC (CASMC) re‐differentiation, and found that G‐1 (selective GPER agonist) induces an enlarged, rectangular/triangular contractile phenotype with increased α‐actin filament density. Further, G‐1 (10−8M – 10−6M) produced a greater increase in SM22α and smooth muscle α‐actin expression compared to controls. Wound‐scratch migration studies demonstrated that G‐1 (24‐hours) inhibited both serum‐ and PDGF‐stimulated migration of porcine CASMC. In addition, G15 (selective GPER antagonist) attenuated the effect of G‐1. These findings suggest that GPER mediates CASMC re‐differentiation and inhibits migration, and could be novel, non‐genomic mechanism whereby estrogen could attenuate the development of coronary atherosclerotic lesions. (Supported by AHA11BGIA7370061)