Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/54651
DC FieldValueLanguage
dc.contributor.authorValbuena-Diez, Ana C.en_US
dc.contributor.authorBlanco, Francisco J.en_US
dc.contributor.authorOujo, Barbaraen_US
dc.contributor.authorLanga, Carmenen_US
dc.contributor.authorGonzalez-Nuñez, Maríaen_US
dc.contributor.authorLlano, Elenaen_US
dc.contributor.authorPendas, Alberto M.en_US
dc.contributor.authorDíaz Sarmiento, María Mercedesen_US
dc.contributor.authorCastrillo, Antonioen_US
dc.contributor.authorLopez-Novoa, José M.en_US
dc.contributor.authorBernabeu, Carmeloen_US
dc.date.accessioned2019-02-18T12:14:47Z-
dc.date.available2019-02-18T12:14:47Z-
dc.date.issued2012en_US
dc.identifier.issn0009-7322en_US
dc.identifier.urihttp://hdl.handle.net/10553/54651-
dc.description.abstractBackground-Ischemia in the placenta is considered the base of the pathogenesis of preeclampsia, a pregnancy-specific syndrome in which soluble endoglin (sEng) is a prognostic marker and plays a pathogenic role. Here, we investigated the effects of hypoxia and the downstream pathways in the release of sEng.Methods and Results-Under hypoxic conditions, the trophoblast-like cell line JAR showed an increase in sEng parallel to an elevated formation of reactive oxygen species. Because reactive oxygen species are related to the formation of oxysterols, we assessed the effect of 22-(R)-hydroxycholesterol, a natural ligand of the liver X receptor (LXR), and the LXR synthetic agonist T0901317. Treatment of JAR cells or human placental explants with 22-(R)-hydroxycholesterol or T0901317 resulted in a clear increase in sEng that was dependent on LXR. These LXR agonists induced an increased matrix metalloproteinase-14 expression and activity and a significant reduction of its endogenous inhibitor, tissue inhibitor of metalloproteinase-3. In addition, mice treated with LXR agonists underwent an increase in the plasma sEng levels, concomitant with an increase in arterial pressure. Moreover, transgenic mice overexpressing sEng displayed high blood pressure. Finally, administration of an endoglin peptide containing the consensus matrix metalloproteinase-14 cleavage site G-L prevented the oxysterol-dependent increase in arterial pressure and sEng levels in mice.Conclusions-These studies provide a clue to the involvement of the LXR pathway in sEng release and its pathogenic role in vascular disorders such as preeclampsia.en_US
dc.languageengen_US
dc.relation.ispartofCirculation (New York, N.Y.)en_US
dc.sourceCirculation [ISSN 0009-7322], v. 126 (22), p. 2612-2624en_US
dc.subject32 Ciencias médicasen_US
dc.subject320108 Ginecologíaen_US
dc.subject2302 Bioquímicaen_US
dc.subject.otherCell hypoxiaen_US
dc.subject.otherHypertensionen_US
dc.subject.otherPreeclampsiaen_US
dc.subject.otherPregnancyen_US
dc.subject.otherPeptidesen_US
dc.titleOxysterol-induced soluble endoglin release and its involvement in hypertensionen_US
dc.typeinfo:eu-repo/semantics/Articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1161/CIRCULATIONAHA.112.101261en_US
dc.identifier.scopus84870248593-
dc.identifier.isi000311492500014-
dc.contributor.authorscopusid55989982900-
dc.contributor.authorscopusid56455387700-
dc.contributor.authorscopusid25951507000-
dc.contributor.authorscopusid6602951087-
dc.contributor.authorscopusid36817686000-
dc.contributor.authorscopusid6603387469-
dc.contributor.authorscopusid35595485200-
dc.contributor.authorscopusid35084829700-
dc.contributor.authorscopusid55445301000-
dc.contributor.authorscopusid7101873361-
dc.contributor.authorscopusid7005583756-
dc.description.lastpage2624en_US
dc.description.firstpage2612en_US
dc.relation.volume126en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.contributor.daisngid9606606-
dc.contributor.daisngid27164407-
dc.contributor.daisngid3114625-
dc.contributor.daisngid1097157-
dc.contributor.daisngid4540202-
dc.contributor.daisngid1389105-
dc.contributor.daisngid399057-
dc.contributor.daisngid5756470-
dc.contributor.daisngid225640-
dc.contributor.daisngid20342-
dc.contributor.daisngid102592-
dc.description.numberofpages13en_US
dc.utils.revisionen_US
dc.contributor.wosstandardWOS:Valbuena-Diez, AC-
dc.contributor.wosstandardWOS:Blanco, FJ-
dc.contributor.wosstandardWOS:Oujo, B-
dc.contributor.wosstandardWOS:Langa, C-
dc.contributor.wosstandardWOS:Gonzalez-Nunez, M-
dc.contributor.wosstandardWOS:Llano, E-
dc.contributor.wosstandardWOS:Pendas, AM-
dc.contributor.wosstandardWOS:Diaz, M-
dc.contributor.wosstandardWOS:Castrillo, A-
dc.contributor.wosstandardWOS:Lopez-Novoa, JM-
dc.contributor.wosstandardWOS:Bernabeu, C-
dc.date.coverdateNoviembre 2012en_US
dc.identifier.ulpgcen_US
dc.contributor.buulpgcBU-MEDen_US
dc.description.sjr7,67
dc.description.jcr15,202
dc.description.sjrqQ1
dc.description.jcrqQ1
dc.description.scieSCIE
item.fulltextSin texto completo-
item.grantfulltextnone-
crisitem.author.deptGIR IUIBS: Medio Ambiente y Salud-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptGIR IUIBS: Farmacología Molecular y Traslacional-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.orcid0000-0002-2057-2159-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameDiaz Sarmiento,Maria Mercedes-
crisitem.author.fullNameCastrillo Viguera, Antonio Jesús-
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