{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T20:23:03Z","timestamp":1790713383796,"version":"4.1.0"},"reference-count":58,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2020,9]]},"abstract":"<jats:sec>\n            <jats:title>Objective:<\/jats:title>\n            <jats:p>ER\u03b1 (estrogen receptor alpha) exerts nuclear genomic actions and also rapid membrane-initiated steroid signaling. The mutation of the cysteine 451 into alanine in vivo has recently revealed the key role of this ER\u03b1 palmitoylation site on some vasculoprotective actions of 17\u03b2-estradiol (E2) and fertility. Here, we studied the in vivo role of the arginine 260 of ER\u03b1 which has also been described to be involved in its E2-induced rapid signaling with PI-3K (phosphoinositide 3-kinase) as well as G protein in cultured cell lines.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results:<\/jats:title>\n            <jats:p>\n              We generated a mouse model harboring a point mutation of the murine counterpart of this arginine into alanine (R264A-ER\u03b1). In contrast to the\n              <jats:italic>C451A-ER\u03b1<\/jats:italic>\n              , the\n              <jats:italic>R264A-ER\u03b1<\/jats:italic>\n              females are fertile with standard hormonal serum levels and normal control of hypothalamus-pituitary ovarian axis. Although R264A-ER\u03b1 protein abundance was normal, the well-described membrane ER\u03b1\u2013dependent actions of estradiol, such as the rapid dilation of mesenteric arteries and the acceleration of endothelial repair of carotid, were abrogated in\n              <jats:italic>R264A-ER\u03b1<\/jats:italic>\n              mice. In striking contrast, E2-regulated gene expression was highly preserved in the uterus and the aorta, revealing intact nuclear\/genomic actions in response to E2. Consistently, 2 recognized nuclear ER\u03b1-dependent actions of E2, namely atheroma prevention and flow-mediated arterial remodeling were totally preserved.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions:<\/jats:title>\n            <jats:p>These data underline the exquisite role of arginine 264 of ER\u03b1 for endothelial membrane-initiated steroid signaling effects of E2 but not for nuclear\/genomic actions. This provides the first model of fertile mouse with no overt endocrine abnormalities with specific loss-of-function of rapid ER\u03b1 signaling in vascular functions.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.120.314159","type":"journal-article","created":{"date-parts":[[2020,7,9]],"date-time":"2020-07-09T09:00:31Z","timestamp":1594285231000},"page":"2143-2158","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":29,"title":["Mutation of Arginine 264 on ER\u03b1 (Estrogen Receptor Alpha) Selectively Abrogates the Rapid Signaling of Estradiol in the Endothelium Without Altering Fertility"],"prefix":"10.1161","volume":"40","author":[{"given":"Marine","family":"Adlanmerini","sequence":"first","affiliation":[{"name":"From the INSERM-UPS UMR U1048, Institut des Maladies M\u00e9taboliques et Cardiovasculaires (M.A., C.F., R.Z., M.B., R.S., T.A., F.B., P.G., H.L., C.F., J.-F.A., F.L.), Universit\u00e9 de Toulouse, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chanaelle","family":"F\u00e9brissy","sequence":"additional","affiliation":[{"name":"From the INSERM-UPS UMR U1048, Institut des Maladies M\u00e9taboliques et Cardiovasculaires (M.A., C.F., R.Z., M.B., R.S., T.A., F.B., P.G., H.L., C.F., J.-F.A., F.L.), Universit\u00e9 de Toulouse, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rana","family":"Zahreddine","sequence":"additional","affiliation":[{"name":"From the INSERM-UPS UMR U1048, Institut des Maladies M\u00e9taboliques et Cardiovasculaires (M.A., C.F., R.Z., M.B., R.S., T.A., F.B., P.G., H.L., C.F., J.-F.A., F.L.), Universit\u00e9 de Toulouse, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emilie","family":"Vessi\u00e8res","sequence":"additional","affiliation":[{"name":"Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale U1083, Centre National de la Recherche Scientifique, Unit\u00e9 Mixte de 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