{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T05:06:03Z","timestamp":1792731963792,"version":"4.5.0"},"reference-count":39,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2001,1,23]]},"abstract":"<jats:p>\n                    <jats:italic>Background<\/jats:italic>\n                    \u2014The atheroprotective effect of 17\u03b2-estradiol (E\n                    <jats:sub>2<\/jats:sub>\n                    ) 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\n                    <jats:sub>2<\/jats:sub>\n                    promotes endothelium-dependent relaxation and accelerates reendothelialization in rats. Similar studies have been undertaken in mice to appreciate the molecular mechanism of this process.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Methods and Results<\/jats:italic>\n                    \u2014We 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\n                    <jats:sub>2<\/jats:sub>\n                    accelerates endothelial regeneration in castrated female wild-type mice. In ovariectomized transgenic mice in which either the estrogen receptor (ER)-\u03b1 or ER\u03b2 gene has been disrupted, E\n                    <jats:sub>2<\/jats:sub>\n                    accelerated reendothelialization in female ER\u03b2 knockout mice, whereas this effect was abolished in female ER\u03b1 knockout mice.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Conclusions<\/jats:italic>\n                    \u2014This study demonstrates that ER\u03b1 but not ER\u03b2 mediates the beneficial effect of E\n                    <jats:sub>2<\/jats:sub>\n                    on reendothelialization and potentially the prevention of atherosclerosis.\n                  <\/jats:p>","DOI":"10.1161\/01.cir.103.3.423","type":"journal-article","created":{"date-parts":[[2012,6,11]],"date-time":"2012-06-11T20:09:32Z","timestamp":1339445372000},"page":"423-428","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":202,"title":["Estradiol Accelerates Reendothelialization in Mouse Carotid Artery Through Estrogen Receptor-\u03b1 but Not Estrogen Receptor-\u03b2"],"prefix":"10.1161","volume":"103","author":[{"given":"L.","family":"Brouchet","sequence":"first","affiliation":[{"name":"From INSERM U397, Institut L. Bugnard, CHU Rangueil, Toulouse (L.B., F.B., J.F.A.), and Institut de Ge\u0301ne\u0301tique et de Biologie Mole\u0301culaire et Cellulaire, CNRS\/INSERM\/ULP\/Colle\u0300ge de France, Illkirch, CU de Strasbourg (A.K., S.D., P.C.), France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Krust","sequence":"additional","affiliation":[{"name":"From INSERM U397, Institut L. Bugnard, CHU Rangueil, Toulouse (L.B., F.B., J.F.A.), and Institut de Ge\u0301ne\u0301tique et de Biologie Mole\u0301culaire et Cellulaire, CNRS\/INSERM\/ULP\/Colle\u0300ge de France, Illkirch, CU de Strasbourg (A.K., S.D., P.C.), France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.","family":"Dupont","sequence":"additional","affiliation":[{"name":"From INSERM U397, Institut L. Bugnard, CHU Rangueil, Toulouse (L.B., F.B., J.F.A.), and Institut de Ge\u0301ne\u0301tique et de Biologie Mole\u0301culaire et Cellulaire, CNRS\/INSERM\/ULP\/Colle\u0300ge de France, Illkirch, CU de Strasbourg (A.K., S.D., P.C.), France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P.","family":"Chambon","sequence":"additional","affiliation":[{"name":"From INSERM U397, Institut L. Bugnard, CHU Rangueil, Toulouse (L.B., F.B., J.F.A.), and Institut de Ge\u0301ne\u0301tique et de Biologie Mole\u0301culaire et Cellulaire, CNRS\/INSERM\/ULP\/Colle\u0300ge de France, Illkirch, CU de Strasbourg (A.K., S.D., P.C.), France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"F.","family":"Bayard","sequence":"additional","affiliation":[{"name":"From INSERM U397, Institut L. Bugnard, CHU Rangueil, Toulouse (L.B., F.B., J.F.A.), and Institut de Ge\u0301ne\u0301tique et de Biologie Mole\u0301culaire et Cellulaire, CNRS\/INSERM\/ULP\/Colle\u0300ge de France, Illkirch, CU de Strasbourg (A.K., S.D., P.C.), France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. F.","family":"Arnal","sequence":"additional","affiliation":[{"name":"From INSERM U397, Institut L. Bugnard, CHU Rangueil, Toulouse (L.B., F.B., J.F.A.), and Institut de Ge\u0301ne\u0301tique et de Biologie Mole\u0301culaire et Cellulaire, CNRS\/INSERM\/ULP\/Colle\u0300ge de France, Illkirch, CU de Strasbourg (A.K., S.D., P.C.), France."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","first-page":"808","volume":"309","year":"1994","unstructured":"Stampfer M, Grodstein F. Cardioprotective effect of hormone replacement therapy is not due to a selection bias. 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