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dc.contributor.authorMendez-Barbero, Nerea 
dc.contributor.authorEsteban, Vanesa 
dc.contributor.authorVillahoz, Silvia 
dc.contributor.authorEscolano, Amelia 
dc.contributor.authorUrso, Katia 
dc.contributor.authorAlfranca, Arantzazu 
dc.contributor.authorRodriguez, Cristina
dc.contributor.authorSanchez, Susana A 
dc.contributor.authorOsawa, Tsuyoshi
dc.contributor.authorAndres, Vicente 
dc.contributor.authorMartinez-Gonzalez, Jose
dc.contributor.authorMinami, Takashi
dc.contributor.authorRedondo, Juan Miguel 
dc.contributor.authorCampanero, Miguel R
dc.date.accessioned2019-05-14T10:00:50Z
dc.date.available2019-05-14T10:00:50Z
dc.date.issued2013-12
dc.identifier.citationEMBO Mol Med. 2013; 5(12):1901-17es_ES
dc.identifier.issn17574676es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7569
dc.description.abstractAtherosclerosis is a complex inflammatory disease involving extensive vascular vessel remodelling and migration of vascular cells. As RCAN1 is implicated in cell migration, we investigated its contribution to atherosclerosis. We show RCAN1 induction in atherosclerotic human and mouse tissues. Rcan1 was expressed in lesional macrophages, endothelial cells and vascular smooth muscle cells and was induced by treatment of these cells with oxidized LDLs (oxLDLs). Rcan1 regulates CD36 expression and its genetic inactivation reduced atherosclerosis extension and severity in Apoe(-/-) mice. This effect was mechanistically linked to diminished oxLDL uptake, resistance to oxLDL-mediated inhibition of macrophage migration and increased lesional IL-10 and mannose receptor expression. Moreover, Apoe(-/-) Rcan1(-/-) macrophages expressed higher-than-Apoe(-/-) levels of anti-inflammatory markers. We previously showed that Rcan1 mediates aneurysm development and that its expression is not required in haematopoietic cells for this process. However, transplantation of Apoe(-/-) Rcan1(-/-) bone-marrow (BM) cells into Apoe(-/-) recipients confers atherosclerosis resistance. Our data define a major role for haematopoietic Rcan1 in atherosclerosis and suggest that therapies aimed at inhibiting RCAN1 expression or function might significantly reduce atherosclerosis burden.es_ES
dc.description.sponsorshipThe Spanish Ministry of Economy and Competitiveness (Ministerio de Economía y Competitividad) supports MRC, JMR and JM‐G with grants SAF2010‐15126, SAF2009‐10708 and SAF2012‐40127, respectively; MRC is also supported by the Spanish Council for Scientific Research (CSIC); JMR is also supported by Fundación La Marató TV3 (080731), and Fundación Genoma España (GENOMA). The Red de Investigacion Cardiovascular (RIC) of the Spanish Ministry of Health (Ministerio de Sanidad) supports the research of JMR, VA and JM‐G with grants RD12/0042/0022, RD12/0042/0028 and RD12/0042/0053, respectively. The Centro Nacional de Investigaciones Cardiovasculares (CNIC) is supported by the Spanish Ministry of Economy and Competitiveness and the Pro‐CNIC Foundation. TM was supported in part by the Leading‐edge Research Promotion Fund (LS038, TM). VE was an investigator of the Sara Borrell Program (CD06/ 00232), and NM‐B holds an FPU fellowship (FPU2008‐1500).es_ES
dc.language.isoenges_ES
dc.publisherEMBO Presses_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectRCAN1es_ES
dc.subjectatherosclerosises_ES
dc.subjecthypercholesterolemiaes_ES
dc.subjectinflammationes_ES
dc.subjectmacrophagees_ES
dc.subject.meshAneurysm es_ES
dc.subject.meshAnimals es_ES
dc.subject.meshApolipoproteins E es_ES
dc.subject.meshAtherosclerosis es_ES
dc.subject.meshBone Marrow Cells es_ES
dc.subject.meshBone Marrow Transplantation es_ES
dc.subject.meshCD36 Antigens es_ES
dc.subject.meshCell Movement es_ES
dc.subject.meshDisease Progression es_ES
dc.subject.meshEndothelial Cells es_ES
dc.subject.meshFoam Cells es_ES
dc.subject.meshHumans es_ES
dc.subject.meshIntracellular Signaling Peptides and Proteins es_ES
dc.subject.meshLipoproteins, LDL es_ES
dc.subject.meshMacrophages es_ES
dc.subject.meshMice es_ES
dc.subject.meshMice, Knockout es_ES
dc.subject.meshMuscle Proteins es_ES
dc.subject.meshMuscle, Smooth, Vasculares_ES
dc.subject.meshPhenotype es_ES
dc.titleA major role for RCAN1 in atherosclerosis progressiones_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID24127415es_ES
dc.format.volume5es_ES
dc.format.number12es_ES
dc.format.page1901-17es_ES
dc.identifier.doi10.1002/emmm.201302842es_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España)es_ES
dc.contributor.funderConsejo Superior de Investigaciones Científicas (España)es_ES
dc.contributor.funderFundación Genoma Españaes_ES
dc.contributor.funderFundación ProCNICes_ES
dc.contributor.funderInstituto de Salud Carlos III - ISCIIIes_ES
dc.description.peerreviewedes_ES
dc.identifier.e-issn1757-4684es_ES
dc.relation.publisherversionhttps://doi.org/10.1002/emmm.201302842es_ES
dc.identifier.journalEMBO molecular medicinees_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Regulación Génica en Remodelado Vascular e Inflamaciónes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Fisiopatología Cardiovascular Molecular y Genéticaes_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2010‐15126es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2009‐10708es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2012‐40127es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RD12/0042/0022es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RD12/0042/0028es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RD12/0042/0053es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/CD06/00232es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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