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dc.contributor.authorVila-Caballer, Marian
dc.contributor.authorGonzalez-Granado, Jose Maria 
dc.contributor.authorZorita, Virginia 
dc.contributor.authorAbu Nabah, Yafa N
dc.contributor.authorSilvestre-Roig, Carlos 
dc.contributor.authordel Monte, Alberto 
dc.contributor.authorMolina-Sanchez, Pedro 
dc.contributor.authorAit-Oufella, Hafid
dc.contributor.authorAndres-Manzano, Maria J. 
dc.contributor.authorSanz, María J
dc.contributor.authorWeber, Christian
dc.contributor.authorKremer, Leonor
dc.contributor.authorGutiérrez, Julio
dc.contributor.authorMallat, Ziad
dc.contributor.authorAndres, Vicente 
dc.date.accessioned2019-06-06T09:51:14Z
dc.date.available2019-06-06T09:51:14Z
dc.date.issued2019-07
dc.identifier.citationJ Mol Cell Cardiol. 2019; 132:154-163es_ES
dc.identifier.issn0022-2828es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7745
dc.description.abstractThe CC chemokine 1 (CCL1, also called I-309 or TCA3) is a potent chemoattractant for leukocytes that plays an important role in inflammatory processes and diseases through binding to its receptor CCR8. Here, we investigated the role of the CCL1-CCR8 axis in atherosclerosis. We found increased expression of CCL1 in the aortas of atherosclerosis-prone fat-fed apolipoprotein E (Apoe)-null mice; moreover, in vitro flow chamber assays and in vivo intravital microscopy demonstrated an essential role for CCL1 in leukocyte recruitment. Mice doubly deficient for CCL1 and Apoe exhibited enhanced atherosclerosis in aorta, which was associated with reduced plasma levels of the anti-inflammatory interleukin 10, an increased splenocyte Th1/Th2 ratio, and a reduced regulatory T cell (Treg) content in aorta and spleen. Reduced Treg recruitment and aggravated atherosclerosis were also detected in the aortas of fat-fed low-density lipoprotein receptor-null mice treated with CCR8 blocking antibodies. These findings demonstrate that disruption of the CCL1-CCR8 axis promotes atherosclerosis by inhibiting interleukin 10 production and Treg recruitment and function.es_ES
dc.description.sponsorshipThis study was supported by the Spanish Ministerio de Ciencia, Innovación y Universidades (MCIU, grants SAF2016-79490-R and SAF2014-57845-R) and the Instituto de Salud Carlos III (ISCIII, grants PI14/00526, PI17/01395, CP11/00145, and CPII16/00022) with co-funding from the European Regional Development Fund (ERDF, “Una manera de hacer Europa”), the Fundación Ramón Areces, European Union (EuroCellNet COST Action CA15214) and the INSERM. VZG is supported by the ISCIII, JMG-G by the ISCIII Miguel Servet Program and the Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), AdMM by the MCIU (predoctoral contract BES-2014-06779), and ZM by a British Heart Foundation Professorship. The CNIC is supported by the MCIU and the Pro CNIC Foundation and is a Severo Ochoa Center of Excellence (SEV-2015-0505).es_ES
dc.language.isoenges_ES
dc.relation.isversionofPostprintes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectAtherosclerosises_ES
dc.subjectCCL1es_ES
dc.subjectCCR8es_ES
dc.subjectIL-10es_ES
dc.subjectTreges_ES
dc.titleDisruption of the CCL1-CCR8 axis inhibits vascular Treg recruitment and function and promotes atherosclerosis in micees_ES
dc.typeArtículoes_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.identifier.pubmedID31121182es_ES
dc.format.volume132es_ES
dc.format.page154-163es_ES
dc.identifier.doi10.1016/j.yjmcc.2019.05.009es_ES
dc.contributor.funderMinisterio de Ciencia, Innovación y Universidades (España)es_ES
dc.contributor.funderInstituto de Salud Carlos III - ISCIIIes_ES
dc.contributor.funderEuropean Regional Development Fund (ERDF/FEDER)es_ES
dc.contributor.funderFundación Ramón Areceses_ES
dc.contributor.funderEuropean Cooperation in Science and Technology. COSTes_ES
dc.contributor.funderBritish Heart Foundationes_ES
dc.contributor.funderFundación ProCNICes_ES
dc.description.peerreviewedes_ES
dc.embargo.terms2020-07-01es_ES
dc.identifier.e-issn1095-8584es_ES
dc.relation.publisherversionhttps://doi.org/10.1016/j.yjmcc.2019.05.009es_ES
dc.identifier.journalJournal of molecular and cellular cardiologyes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Fisiopatología Cardiovascular Molecular y Genéticaes_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2016-79490-Res_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2014-57845-Res_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI14/00526es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI17/01395es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/CP11/00145es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/CPII16/00022es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/BES-2014-06779es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SEV-2015-0505es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/embargoedAccesses_ES


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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
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