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Circulation. 2001;103:423-428

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(Circulation. 2001;103:423.)
© 2001 American Heart Association, Inc.


Basic Science Reports

Estradiol Accelerates Reendothelialization in Mouse Carotid Artery Through Estrogen Receptor-{alpha} but Not Estrogen Receptor-ß

L. Brouchet, MD; A. Krust, PhD; S. Dupont, PhD; P. Chambon, PhD; F. Bayard, MD, PhD; J. F. Arnal, MD, PhD

From INSERM U397, Institut L. Bugnard, CHU Rangueil, Toulouse (L.B., F.B., J.F.A.), and Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP/Collège de France, Illkirch, CU de Strasbourg (A.K., S.D., P.C.), France.

Correspondence to J.F. Arnal, INSERM U397, Institut L. Bugnard, CHU Rangueil, 31403 Toulouse, France. E-mail arnal{at}rangueil.inserm.fr

Background—The atheroprotective effect of 17ß-estradiol (E2) 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 E2 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 E2 accelerates endothelial regeneration in castrated female wild-type mice. In ovariectomized transgenic mice in which either the estrogen receptor (ER)-{alpha} or ERß gene has been disrupted, E2 accelerated reendothelialization in female ERß knockout mice, whereas this effect was abolished in female ER{alpha} knockout mice.

Conclusions—This study demonstrates that ER{alpha} but not ERß mediates the beneficial effect of E2 on reendothelialization and potentially the prevention of atherosclerosis.


Key Words: hormones • receptors • arteries • endothelium




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