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.
dc.contributor.authorBlanco, Francisco J.
dc.contributor.authorOujo, Barbara
dc.contributor.authorLanga, Carmen
dc.contributor.authorGonzalez-Nuñez, María
dc.contributor.authorLlano, Elena
dc.contributor.authorPendas, Alberto M.
dc.contributor.authorDíaz, Mercedes
dc.contributor.authorCastrillo, Antonio
dc.contributor.authorLopez-Novoa, José M.
dc.contributor.authorBernabeu, Carmelo
dc.date.accessioned2019-02-18T12:14:47Z-
dc.date.available2019-02-18T12:14:47Z-
dc.date.issued2012
dc.identifier.issn0009-7322
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. (Circulation. 2012;126:2612-2624.)
dc.publisher0009-7322
dc.relation.ispartofCirculation (New York, N.Y.)
dc.sourceCirculation[ISSN 0009-7322],v. 126, p. 2612-2624
dc.subject.otherLiver-X-Receptors
dc.subject.otherGrowth-Factor-Beta
dc.subject.otherHuman Choriocarcinoma Cells
dc.subject.otherHuman Trophoblast Invasion
dc.subject.otherNuclear Receptors
dc.subject.otherLxr-Alpha
dc.subject.otherEndothelial-Cells
dc.subject.otherPreeclampsia
dc.subject.otherCholesterol
dc.subject.otherExpression
dc.titleOxysterol-induced soluble endoglin release and its involvement in hypertension
dc.typeinfo:eu-repo/semantics/Article
dc.typeArticle
dc.identifier.doi10.1161/CIRCULATIONAHA.112.101261
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.lastpage2624
dc.description.firstpage2612
dc.relation.volume126
dc.type2Artículo
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.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 2012
dc.identifier.ulpgces
item.fulltextSin texto completo-
item.grantfulltextnone-
crisitem.author.orcid0000-0003-3878-3867-
crisitem.author.fullNameDiaz Cabrera, Moises-
crisitem.author.fullNameCastrillo Viguera, Antonio Jesús-
Appears in Collections:Artículos
Show simple item record

SCOPUSTM   
Citations

64
checked on May 16, 2021

WEB OF SCIENCETM
Citations

68
checked on May 16, 2021

Page view(s)

6
checked on May 15, 2021

Google ScholarTM

Check

Altmetric


Share



Export metadata



Items in accedaCRIS are protected by copyright, with all rights reserved, unless otherwise indicated.