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. Author manuscript; available in PMC: 2014 Nov 24.
Published in final edited form as: Alcohol Clin Exp Res. 2011 May 20;35(9):1686–1693. doi: 10.1111/j.1530-0277.2011.01515.x

Figure 3. Interactive effects of estradiol-17β and alcohol on uterine arterial endothelial proliferative function.

Figure 3

(A) Estradiol 17β-induced uterine artery endothelial cell (UAEC) proliferative response in the lower dose (LD) alcohol group compared to the controls (Ctrl). Dose-dependent proliferative effects of estradiol-17β that we previously reported (Jobe et al., 2010) were abolished by alcohol. The presence of LD alcohol with estradiol-17β significantly (*) decreased proliferation independent of whether the cells were previously exposed to binge-like LD alcohol. Specifically, the estradiol-17β-induced proliferation was significantly decreased in the binge-like LD alcohol group even if alcohol was not present with estradiol-17β in the system. However, this decrease ($) was significantly lower compared to when alcohol was present with estradiol-17β. (B) Estradiol-17β-induced proliferative response in the higher dose (HD) group compared to the Ctrl. Similar to the LD group, the presence of HD alcohol with estradiol-17β significantly decreased (*) proliferation independent of whether the cells were previously exposed to binge-like HD alcohol. However, unlike the LD group, there was no difference in the binge-like HD alcohol groups even if alcohol was not present with estradiol-17β in the system compared to when alcohol was present.