17beta-estradiol accelerates endothelial regeneration in female mice following carotid injury, an effect mediated by estrogen receptor-alpha but not estrogen receptor-beta.
Does 17beta-estradiol accelerate reendothelialization in a mouse model of carotid injury, and which estrogen receptor mediates this effect?
17beta-estradiol accelerates reendothelialization following carotid injury specifically via estrogen receptor-alpha, providing mechanistic insight into its potential atheroprotective effects.
BACKGROUND: The atheroprotective effect of 17beta-estradiol (E(2)) has been suggested in women and clearly demonstrated in animals through both an effect on lipid metabolism and a direct effect on the cells of the arterial wall. It has been shown, for example, that E(2) promotes endothelium-dependent relaxation and accelerates reendothelialization in rats. Similar studies have been undertaken in mice to appreciate the molecular mechanism of this process. METHODS AND RESULTS: We report here a model of electric carotid injury adapted from that described by Carmeliet et al (1997) that allows us to precisely evaluate the reendothelialization process. We demonstrate that E(2) accelerates endothelial regeneration in castrated female wild-type mice. In ovariectomized transgenic mice in which either the estrogen receptor (ER)-alpha or ERbeta gene has been disrupted, E(2) accelerated reendothelialization in female ERbeta knockout mice, whereas this effect was abolished in female ERalpha knockout mice. CONCLUSIONS: This study demonstrates that ERalpha but not ERbeta mediates the beneficial effect of E(2) on reendothelialization and potentially the prevention of atherosclerosis.
Brouchet et al. (Tue,) conducted a other in Electric carotid injury. 17beta-estradiol (E2) was evaluated on Reendothelialization. 17beta-estradiol accelerates endothelial regeneration in female mice following carotid injury, an effect mediated by estrogen receptor-alpha but not estrogen receptor-beta.