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dc.contributor.authorTabruyn, Sebastien P.-
dc.contributor.authorHansen, Sylvain-
dc.contributor.authorOjeda-Fernández, María Luisa-
dc.contributor.authorBovy, Nicolas-
dc.contributor.authorZarrabeitia, Roberto-
dc.contributor.authorRecio-Poveda, Lucía-
dc.contributor.authorBernabéu, Carmelo-
dc.contributor.authorMartial, Joseph A.-
dc.contributor.authorBotella, Luisa María-
dc.contributor.authorStruman, Ingrid-
dc.date.accessioned2014-07-24T08:20:17Z-
dc.date.available2014-07-24T08:20:17Z-
dc.date.issued2013-06-26-
dc.identifier.citationAngiogenesis 16 (4) 877-887 (2013)es_ES
dc.identifier.issn0969-6970-
dc.identifier.urihttp://hdl.handle.net/10261/100430-
dc.description20 p.-6 fig.es_ES
dc.description.abstractHereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant disorder characterized by arteriovenous malformations and hemorrhages. This vascular disease results mainly from mutations in 2 genes involved in the TGF-β pathway (ENG and ALK1) that are exclusively expressed by endothelial cells. The present study identified miR-27a and miR-205 as two circulating miRNAs differentially expressed in HHT patients. The plasma levels of miR-27a are elevated while those of miR-205 are reduced in both HHT1 and HHT2 patients compared to healthy controls. The role of miR-205 in endothelial cells was further investigated. Our data indicates that miR-205 expression displaces the TGF-β balance towards the anti-angiogenic side by targeting Smad1 and Smad4. In line, overexpression of miR-205 in endothelial cells reduces proliferation, migration and tube formation while its inhibition shows opposite effects. This study not only suggests that detection of circulating miRNA (miR-27a and miR-205) could help for the screening of HHT patients but also provides a functional link between the deregulated expression of miR-205 and the HHT phenotype. © 2013 Springer Science+Business Media Dordrecht.es_ES
dc.description.sponsorshipThis study was supported by the University of Liège (Fonds Speciaux), le centre anti-cancéreux (CAC ULg), the FRIA (Fonds pour la Recherche Industrielle et Agricole, Belgium), the FNRS (Fonds National de la Recherche Scientifique, Belgium), the Neoangio program #616476 of the “Service Public de Wallonie”. This work was supported by the Ministerio de Ciencia e Innovacion: Grants SAF2008–01218, SAF2011-23475, SAF2007–61827, and SAF2010–19222, and Fundación Ramón Areces of Spain (Rare and Emergent Diseases).es_ES
dc.language.isoenges_ES
dc.publisherSpringeres_ES
dc.relation.isversionofPostprintes_ES
dc.rightsopenAccesses_ES
dc.subjectHereditary hemorrhagic telangiectasiaes_ES
dc.subjectMicroRNAes_ES
dc.subjectTGF-betaes_ES
dc.titleMiR-205 is downregulated in hereditary hemorrhagic telangiectasia and impairs TGF-beta signaling pathways in endothelial cellses_ES
dc.typeartículoes_ES
dc.identifier.doi10.1007/s10456-013-9362-9-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttp://dx.doi.org/10.1007/s10456-013-9362-9es_ES
dc.identifier.e-issn1573-7209-
dc.relation.csices_ES
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