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dc.contributor.authorDel Toro, Raquel 
dc.contributor.authorChevre, Raphael 
dc.contributor.authorRodriguez, Cristina
dc.contributor.authorOrdonez, Antonio
dc.contributor.authorMartinez-Gonzalez, Jose
dc.contributor.authorAndres, Vicente 
dc.contributor.authorMendez-Ferrer, Simon 
dc.date.accessioned2017-10-20T10:33:52Z
dc.date.available2017-10-20T10:33:52Z
dc.date.issued2016
dc.identifierISI:000384973300001
dc.identifier.citationNat Commun. 2016; 7:12706
dc.identifier.issn2041-1723
dc.identifier.urihttp://hdl.handle.net/20.500.12105/5185
dc.description.abstractAtherosclerosis is a leading death cause. Endothelial and smooth muscle cells participate in atherogenesis, but it is unclear whether other mesenchymal cells contribute to this process. Bone marrow (BM) nestin(+) cells cooperate with endothelial cells in directing monocyte egress to bloodstream in response to infections. However, it remains unknown whether nestin(+) cells regulate inflammatory cells in chronic inflammatory diseases, such as atherosclerosis. Here, we show that nestin(+) cells direct inflammatory cell migration during chronic inflammation. In Apolipoprotein E (ApoE) knockout mice fed with high-fat diet, BM nestin(+) cells regulate the egress of inflammatory monocytes and neutrophils. In the aorta, nestin(+) stromal cells increase similar to 30 times and contribute to the atheroma plaque. Mcp1 deletion in nestin(+) cells-but not in endothelial cells only-increases circulating inflammatory cells, but decreases their aortic infiltration, delaying atheroma plaque formation and aortic valve calcification. Therefore, nestin expression marks cells that regulate inflammatory cell migration during atherosclerosis.
dc.description.sponsorshipWe thank EG Pamer, GN Enikolopov, G Fishell and RH Adams for donating mice. X Langa, S Martin-Salamanca, D Martin-Perez, R Villa-Bellosta, I Bilbao, J Ruiz-Cabello, AM Martin, AB Ricote, JM Ligos, R Nieto, A Benitez and the CNIC Comparative Medicine, Cellomics and Microscopy Units for assistance, and other members of S.M-F. lab for helpful discussions. This work was supported by core support grants from the Pro-CNIC Foundation, Severo Ochoa Center of Excellence award SEV-2015-0505 to CNIC, and the Wellcome Trust and MRC to the Cambridge Stem Cell Institute, Spanish Ministry of Economy and Competitiveness (RETIC Grant RD12/0042/0028 to V.A.; SAF2012-40127 to J.M-G.; Plan Nacional Grant SAF-2011-30308, Ramon y Cajal Program Grant RYC-2009-04703 and Spanish Cell Therapy Network TerCel to S.M-F.); Marie Curie Career Integration Program Grant (FP7-PEOPLE-2011-294096) and ConSEPOC-Comunidad de Madrid Grant (S2010/BMD-2542), National Health Institute Blood and Transplant (United Kingdom), Horizon2020 (ERC-2014-CoG-64765) and an International Early Career Scientist grant of the Howard Hughes Medical Institute to S.M-F.
dc.language.isoeng
dc.publisherNature Publishing Group 
dc.type.hasVersionVoR
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectMYELOID CALCIFYING CELLS
dc.subjectSMOOTH-MUSCLE-CELLS
dc.subjectPROGENITOR CELLS
dc.subjectVASA-VASORUM
dc.subjectSTEM-CELLS
dc.subjectHEMATOPOIETIC STEM
dc.subjectMONOCYTE RECRUITMENT
dc.subjectNEOINTIMA FORMATION
dc.subjectENDOTHELIAL-CELLS
dc.subjectMESENCHYMAL STEM
dc.titleNestin(+) cells direct inflammatory cell migration in atherosclerosis
dc.typejournal article
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID27586429
dc.format.volume7
dc.identifier.doi10.1038/ncomms12706
dc.contributor.funderFundación ProCNIC 
dc.contributor.funderMinisterio de Economía y Competitividad (España) 
dc.contributor.funderWellcome Trust 
dc.contributor.funderMRC Cambridge Stem Cell Institute 
dc.contributor.funderComunidad de Madrid (España) 
dc.contributor.funderUnión Europea. Comisión Europea 
dc.contributor.funderHoward Hughes Medical Institute 
dc.contributor.funderNHS - Blood and Transplant (NHSBT) (Reino Unido) 
dc.description.peerreviewed
dc.relation.publisherversionhttps://doi.org/10.1038/ncomms12706
dc.identifier.journalNature Communications
dc.repisalud.orgCNICCNIC::Grupos de investigación::Fisiopatología Cardiovascular Molecular y Genética
dc.repisalud.orgCNICCNIC::Grupos de investigación::Antiguos CNIC
dc.repisalud.institucionCNIC
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/FP7/294096/EUes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SEV-2015-0505es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/H2020/64765es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2012-40127es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF-2011-30308es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RYC-2009-04703es_ES
dc.rights.accessRightsopen accesses_ES


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