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dc.contributor.authorGonzalez-Hernández, Sara 
dc.contributor.authorGomez, Manuel J 
dc.contributor.authorSanchez-Cabo, Fatima 
dc.contributor.authorMendez-Ferrer, Simon 
dc.contributor.authorMunoz-Canoves, Pura 
dc.contributor.authorIsern, Joan 
dc.date.accessioned2020-11-27T16:19:13Z
dc.date.available2020-11-27T16:19:13Z
dc.date.issued2020-11-06
dc.identifier.citationCirc Res. 2020; 127(11):e252-270es_ES
dc.identifier.issn0009-7330
dc.identifier.urihttp://hdl.handle.net/20.500.12105/11462
dc.description.abstractThe molecular mechanisms underlying the formation of coronary arteries during development and during cardiac neovascularization after injury are poorly understood. However, a detailed description of the relevant signaling pathways and functional TFs (transcription factors) regulating these processes is still incomplete. The goal of this study is to identify novel cardiac transcriptional mechanisms of coronary angiogenesis and vessel remodeling by defining the molecular signatures of coronary vascular endothelial cells during these complex processes. We demonstrate that Nes-gfp and Nes-CreER T2 transgenic mouse lines are novel tools for studying the emergence of coronary endothelium and targeting sprouting coronary vessels (but not ventricular endocardium) during development. Furthermore, we identify Sox17 as a critical TF upregulated during the sprouting and remodeling of coronary vessels, visualized by a specific neural enhancer from the Nestin gene that is strongly induced in developing arterioles. Functionally, genetic-inducible endothelial deletion of Sox17 causes deficient cardiac remodeling of coronary vessels, resulting in improper coronary artery formation. We demonstrated that Sox17 TF regulates the transcriptional activation of Nestin's enhancer in developing coronary vessels while its genetic deletion leads to inadequate coronary artery formation. These findings identify Sox17 as a critical regulator for the remodeling of coronary vessels in the developing heart.es_ES
dc.description.sponsorshipThis work was supported by grants from the Spanish Ministerio de Economía y Competitividad (BFU2012-35892 and Ramón y Cajal Program grant RYC-2011-09209 to J.I.), and FPIMINECO13fellowship (BES-2013-065514) to S.G.H. Additionally, S.M.-F laboratory received funding from PlanNacional grant SAF-2011-30308, Ramón y Cajal Program grant RYC-2009-04703, Spanish CellTherapy Network TerCel, Marie Curie Career Integration Program grant FP7-PEOPLE-2011-RG-294096, ConSEPOC-Comunidad de Madrid grant S2010/BMD-2542 and Howard Hughes International Early Career Scientist grant. This study was also supported by Intramural grants from the Severo Ochoa program (IGP-SO), Fundació La Marató de TV3 (120/C/2015-20153032), and grant RTI2018-095497-B-I00 from MCIU to A.H.; and to MINECO RTI2018-096068, AFM, MDA, LaCaixa-HR17-00040, UPGRADE-H2020-825825 grants and ERC Advanced Grant-741538 to PMC. The CNIC is supported by the Instituto de Salud Carlos III (ISCIII), the Ministerio de Ciencia e Innovación (MCIN) and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (SEV-2015-0505). The UPF is a María de Maeztu Unit of Excellence (MDM-2014-0370).es_ES
dc.language.isoenges_ES
dc.publisherAmerican Heart Association (AHA) es_ES
dc.relation.isversionofPostprintes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.titleSox17 Controls Emergence and Remodeling of Nestin-Expressing Coronary Vessels.es_ES
dc.typeArtículoes_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.identifier.pubmedID32921258es_ES
dc.format.volume127es_ES
dc.format.number11es_ES
dc.format.pagee252-e270es_ES
dc.identifier.doi10.1161/CIRCRESAHA.120.317121es_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España)
dc.contributor.funderEuropean Commission 
dc.contributor.funderComunidad de Madrid 
dc.contributor.funderHoward Hughes Medical Institute
dc.contributor.funderFundació La Marató
dc.contributor.funderMinisterio de Ciencia, Innovación y Universidades (España)
dc.contributor.funderFundación La Caixa
dc.contributor.funderInstituto de Salud Carlos III 
dc.contributor.funderMinisterio de Ciencia e Innovación (España)
dc.contributor.funderFundación ProCNIC
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.1161/CIRCRESAHA.120.317121es_ES
dc.identifier.journalCirculation researches_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Laboratorio de Regeneración Tisulares_ES
dc.repisalud.orgCNICCNIC::Unidades técnicas::Bioinformáticaes_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SEV-2015-0505es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/BFU2012-35892es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RYC-2011-09209es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/BES-2013-065514es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF-2011-30308es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RYC-2009-04703es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/FP7/294096es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RTI2018-095497-B-I00es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RTI2018-096068es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/H2020/741538es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/MDM-2014-0370es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/embargoedAccesses_ES


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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
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