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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, RESULTS. Meshes: Animals, Arteriosclerosis, Carotid Artery Injuries, Carotid Artery, Common, Castration, Disease Models, Animal, Endothelium, Vascular, Estradiol, Estrogen Receptor alpha, Estrogen Receptor beta, Evans Blue, Female, Mice, Mice, Inbred C57BL, Mice, Knockout, Microscopy, Electron, Scanning, Receptors, Estrogen, Regeneration, Staining and Labeling, Time Factors.
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Does estradiol accelerate reendothelialization in mouse carotid artery through estrogen receptor-alpha but not estrogen receptor-beta? Context: 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. 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.
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This study demonstrates that ERalpha but not ERbeta mediates the beneficial effect of E(2) on reendothelialization and potentially the prevention of atherosclerosis. Final Decision: yes