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Combined deficiency of Notch1 and Notch3 causes pericyte dysfunction, models CADASIL, and results in arteriovenous malformations.

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dc.contributor.authorKofler, Natalie M
dc.contributor.authorCuervo, Henar
dc.contributor.authorUh, Minji K
dc.contributor.authorMurtomäki, Aino
dc.contributor.authorKitajewski, Jan
dc.date.accessioned2024-01-17T14:20:17Z
dc.date.available2024-01-17T14:20:17Z
dc.date.issued2015-11-13
dc.description.abstractPericytes regulate vessel stability and pericyte dysfunction contributes to retinopathies, stroke, and cancer. Here we define Notch as a key regulator of pericyte function during angiogenesis. In Notch1(+/-); Notch3(-/-) mice, combined deficiency of Notch1 and Notch3 altered pericyte interaction with the endothelium and reduced pericyte coverage of the retinal vasculature. Notch1 and Notch3 were shown to cooperate to promote proper vascular basement membrane formation and contribute to endothelial cell quiescence. Accordingly, loss of pericyte function due to Notch deficiency exacerbates endothelial cell activation caused by Notch1 haploinsufficiency. Mice mutant for Notch1 and Notch3 develop arteriovenous malformations and display hallmarks of the ischemic stroke disease CADASIL. Thus, Notch deficiency compromises pericyte function and contributes to vascular pathologies.es_ES
dc.description.peerreviewedSíes_ES
dc.format.page16449es_ES
dc.format.volume5es_ES
dc.identifier.citationSci Rep. 2015 Nov 13:5:16449.es_ES
dc.identifier.doi10.1038/srep16449es_ES
dc.identifier.e-issn2045-2322es_ES
dc.identifier.journalScientific reportses_ES
dc.identifier.pubmedID26563570es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/17218
dc.language.isoenges_ES
dc.publisherNature Publishing Groupes_ES
dc.relation.publisherversion10.1038/srep16449es_ES
dc.repisalud.institucionCNICes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Genética Molecular de la Angiogénesises_ES
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.meshAnimalses_ES
dc.subject.meshArteriovenous Malformationses_ES
dc.subject.meshBlotting, Westernes_ES
dc.subject.meshCADASILes_ES
dc.subject.meshCell Differentiationes_ES
dc.subject.meshCells, Culturedes_ES
dc.subject.meshDisease Models, Animales_ES
dc.subject.meshEndothelial Cellses_ES
dc.subject.meshGene Expressiones_ES
dc.subject.meshHEK293 Cellses_ES
dc.subject.meshHumanses_ES
dc.subject.meshMatrix Metalloproteinase 2es_ES
dc.subject.meshMice, Inbred C57BLes_ES
dc.subject.meshMice, Knockoutes_ES
dc.subject.meshMicroscopy, Confocales_ES
dc.subject.meshMicroscopy, Electron, Transmissiones_ES
dc.subject.meshMuscle, Smooth, Vasculares_ES
dc.subject.meshPericyteses_ES
dc.subject.meshReceptor, Notch1es_ES
dc.subject.meshReceptor, Notch3es_ES
dc.subject.meshReceptor, Platelet-Derived Growth Factor betaes_ES
dc.subject.meshReceptors, Notches_ES
dc.subject.meshRetinal Vesselses_ES
dc.subject.meshReverse Transcriptase Polymerase Chain Reactiones_ES
dc.subject.meshTime Factorses_ES
dc.titleCombined deficiency of Notch1 and Notch3 causes pericyte dysfunction, models CADASIL, and results in arteriovenous malformations.es_ES
dc.typejournal articlees_ES
dc.type.hasVersionVoRes_ES
dspace.entity.typePublication
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