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Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/51792
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dc.contributor.authorBaquié, Mathurin-
dc.contributor.authorCobo-Vuilleumier, Nadia-
dc.contributor.authorLorenzo, Petra Isabel-
dc.contributor.authorJiménez-Moreno, Carmen M.-
dc.contributor.authorGauthier, Benoit R.-
dc.date.accessioned2012-06-18T13:31:00Z-
dc.date.available2012-06-18T13:31:00Z-
dc.date.issued2011-07-15-
dc.identifierissn: 0964-6906-
dc.identifiere-issn: 1460-2083-
dc.identifier.citationHuman Molecular Genetics 20(14): 2823-2833 (2011)-
dc.identifier.urihttp://hdl.handle.net/10261/51792-
dc.descriptionet al.-
dc.description.abstractLiver receptor homolog (LRH-1) is an orphan nuclear receptor (NR5A2) that regulates cholesterol homeostasis and cell plasticity in endodermal-derived tissues. Estrogen increases LRH-1 expression conveying cell protection and proliferation. Independently, estrogen also protects isolated human islets against cytokine- induced apoptosis. Herein, we demonstrate that LRH-1 is expressed in islets, including β-cells, and that transcript levels are modulated by 17β-estradiol through the estrogen receptor (ER)α but not ERβ signaling pathway. Repression of LRH-1 by siRNA abrogated the protective effect conveyed by estrogen on rat islets against cytokines. Adenoviral-mediated overexpression of LRH-1 in human islets did not alter proliferation but conferred protection against cytokines and streptozotocin-induced apoptosis. Expression levels of the cell cycle genes cyclin D1 and cyclin E1 as well as the antiapoptotic gene bcl-xl were unaltered in LRH-1 expressing islets. In contrast, the steroidogenic enzymes CYP11A1 and CYP11B1 involved in glucocorticoid biosynthesis were both stimulated in transduced islets. In parallel, graded overexpression of LRH-1 dose- dependently impaired glucose-induced insulin secretion. Our results demonstrate the crucial role of the estrogen target gene nr5a2 in protecting human islets against-stressed-induced apoptosis. We postulate that this effect is mediated through increased glucocorticoid production that blunts the pro-inflammatory response of islets. © The Author 2011. Published by Oxford University Press. All rights reserved.-
dc.description.sponsorshipThis work was supported by grants from the Swiss National Science Foundation (310030-119763 to B.R.G., 310000-116750/1 to C.B.W., 32003B-120376 to D.B.), the Juvenile Diabetes Research Foundation (9-2004-384 to E.C.I.T.), the Fundacion Progreso y Salud (to B.R.G.) and the Junta de Andalucia, Consejeria de Salud (PI-0727-2010 to B.R.G.).-
dc.language.isoeng-
dc.publisherOxford University Press-
dc.rightsclosedAccess-
dc.titleThe liver receptor homolog-1 (LRH-1) is expressed in human islets and protects β-cells against stress-induced apoptosis-
dc.typeartículo-
dc.identifier.doi10.1093/hmg/ddr193-
dc.date.updated2012-06-18T13:31:01Z-
dc.description.versionPeer Reviewed-
dc.contributor.funderSwiss National Science Foundation-
dc.contributor.funderJuvenile Diabetes Research Foundation International-
dc.contributor.funderJunta de Andalucía-
dc.contributor.funderFundación Progreso y Salud-
dc.relation.csicSí-
dc.identifier.funderhttp://dx.doi.org/10.13039/100000901es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100011011es_ES
dc.type.coarhttp://purl.org/coar/resource_type/c_6501es_ES
item.openairetypeartículo-
item.grantfulltextnone-
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
item.languageiso639-1en-
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