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. Author manuscript; available in PMC: 2016 Aug 1.
Published in final edited form as: J Endocrinol. 2015 Aug 24;227(1):61–69. doi: 10.1530/JOE-15-0257

Figure 1.

Figure 1

Role of GPER in estrogen-dependent inhibition of thromboxane A2 production in human endothelial cells. Endothelial cells were treated with 17β-estradiol (E2, 100 nmol/L), the GPER-selective antagonist G36 (1 μmol/L), or solvent (DMSO 0.01%) for 24 hours, and thromboxane A2 production was measured under basal conditions or after concomitant stimulation with the pro-inflammatory cytokine TNF-α (1 ng/mL). *P<0.05 vs. basal; †P<0.05 vs. solvent; #P<0.05 vs. 17β-estradiol. All data (n=3 independent experiments per group) are mean±s.e.m.