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dc.contributor.authorPontes-Quero, Samuel 
dc.contributor.authorFernandez-Chacon, Macarena 
dc.contributor.authorLuo, Wen 
dc.contributor.authorLunella, Federica Francesca 
dc.contributor.authorCasquero-Garcia, Veronica 
dc.contributor.authorGarcia-Gonzalez, Irene 
dc.contributor.authorHermoso, Ana 
dc.contributor.authorRocha, Susana 
dc.contributor.authorBansal, Mayank 
dc.contributor.authorBenedito, Rui 
dc.date.accessioned2019-05-07T07:55:10Z
dc.date.available2019-05-07T07:55:10Z
dc.date.issued2019-05-01
dc.identifier.citationNat Commun. 2019; 10(1):2016es_ES
dc.identifier.issn2041-1723es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7542
dc.description.abstractAppropriate therapeutic modulation of endothelial proliferation and sprouting is essential for the effective inhibition of angiogenesis in cancer or its induction in cardiovascular disease. The current view is that an increase in growth factor concentration, and the resulting mitogenic activity, increases both endothelial proliferation and sprouting. Here, we modulate mitogenic stimuli in different vascular contexts by interfering with the function of the VEGF and Notch signalling pathways at high spatiotemporal resolution in vivo. Contrary to the prevailing view, our results indicate that high mitogenic stimulation induced by VEGF, or Notch inhibition, arrests the proliferation of angiogenic vessels. This is due to the existence of a bell-shaped dose-response to VEGF and MAPK activity that is counteracted by Notch and p21, determining whether endothelial cells sprout, proliferate, or become quiescent. The identified mechanism should be considered to achieve optimal therapeutic modulation of angiogenesis.es_ES
dc.description.sponsorshipResearch in the R.B. group was supported by the European Research Council (ERC-2014-StG—638028), the Centro Nacional de Investigaciones Cardiovasculares (CNIC), and by the Ministerio de Economia, Industria y Competitividad (MEIC: SAF2013-44329-P, SAF2013-42359-ERC and RYC-2013-13209). The CNIC is supported by the Ministerio de Ciencia, Innovación y Universidades (MCNU) and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (SEV-2015–0505). S. Pontes-Quero and M. Fernandez-Chacon received PhD fellowships from the La Caixa bank. W. Luo received a COFUND CNIC International Postdoctoral fellowship.es_ES
dc.language.isoenges_ES
dc.publisherNature Publishing Group es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.titleHigh mitogenic stimulation arrests angiogenesises_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID31043605es_ES
dc.format.volume10es_ES
dc.format.number1es_ES
dc.format.page2016es_ES
dc.identifier.doi10.1038/s41467-019-09875-7es_ES
dc.contributor.funderUnión Europea. Comisión Europea 
dc.contributor.funderUnión Europea. Comisión Europea. European Research Council (ERC) 
dc.contributor.funderMinisterio de Economía, Industria y Competitividad (España) 
dc.contributor.funderMinisterio de Ciencia, Innovación y Universidades (España) 
dc.contributor.funderFundación ProCNIC 
dc.contributor.funderFundación La Caixa 
dc.description.peerreviewedes_ES
dc.identifier.e-issn2041-1723es_ES
dc.relation.publisherversionhttps://doi.org/10.1038/s41467-019-09875-7es_ES
dc.identifier.journalNature communicationses_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Genética Molecular de la Angiogénesises_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/H2020/638028es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SEV-2015-0505es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2013-44329-Pes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2013-42359-ERCes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RYC-2013-13209es_ES
dc.rights.accessRightsopen accesses_ES


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