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(Circulation. 2001;103:423.)
© 2001 American Heart Association, Inc.
Basic Science Reports |
but Not Estrogen Receptor-ß
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
BackgroundThe 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 ResultsWe
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)-
or ERß gene has been
disrupted, E2 accelerated reendothelialization
in female ERß knockout mice, whereas this effect was abolished in
female ER
knockout mice.
ConclusionsThis study
demonstrates that ER
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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