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. 2013 Dec 26;111(2):E283–E290. doi: 10.1073/pnas.1322057111

Fig. 5.

Fig. 5.

Membrane-initiated endothelial effects of E2 are abrogated in C451A-ERα mice. (A) Percentage of relaxation of mesenteric arteries from WT-C451, ERα −/−, and C451A-ERα mice following addition of E2 (1 µM) or EDC (ethinyl-estradiol dendrimer conjugate, 1 µM), n = 8–9. (B) Phospho-eNOS/eNOS abundance in carotid arteries from WT-C451, ERα −/−, and C451A-ERα mice treated or not with E2 (10−8 M, 30 min), n = 6. Representative Western blot is shown. AU, arbitrary units. (C) Percentage of migration of primary endothelial cells treated or not with E2 (10−9 M, 16 h), n = 3–4. (D) Carotid artery reendothelialization in ovariectomized WT-C451 and C451A-ERα mice treated or not with E2 (80 µg⋅kg–1⋅d–1, 2 wk), n = 8–10. For C and D, statistical results of two-way ANOVA are shown, reporting the statistical interaction between treatment and genotype.