Activation of G-protein-coupled estrogen receptor (GPER) inhibits coronary artery smooth muscle cell proliferation Conference Paper uri icon


  • One aspect of the beneficial influences of 17estradiol on vascular smooth muscle cells (VSMC) is inhibition of VSMC proliferation following vascular injury. GPER is a potential mediator of estrogen action on coronary arteries, but whether GPER plays a role in coronary artery smooth muscle proliferation has never been reported. The objective of our study was to test the functional role of GPER in human and porcine coronary (CASMC) proliferation by applying flow cytometric analysis and Western blotting. The results are as follows: G1 (GPER agonist) inhibited both human and porcine CASMC proliferation in a concentration and timedependent manner (108 to 105 M). Flow cytometry revealed that G1 significantly decreased the proportion of Sphase and G2/M cells in the growing cell population (stimulated by 10% charcoal/dextron striped FBS or 10 nM PDGFBB), suggesting that G1induces cell proliferation by slowing down the progression of the cell cycle. Western blot revealed that G1induced cell cycle retardation was associated with decreased expression of cyclinB, upregulation of cyclinD1, and concomitant induction of p21. G1 treatment also inhibited the phosphorylation of ERK1/2 and Akt. We conclude that GPER activation inhibits CASMC proliferation by retardation of cell cycle progression via inhibiting ERK1/2 and Akt activities.

published proceedings


author list (cited authors)

  • Li, F., Wang, G., Zhou, B., White, R., Heaps, C., Stallone, J., & Han, G.

citation count

  • 0

complete list of authors

  • Li, Fen||Wang, Gang||Zhou, Beiyan||White, Richard||Heaps, Cristine||Stallone, John||Han, Guichun

publication date

  • April 2012