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dc.contributor.authorGonzález-Ramos, Silvia
dc.contributor.authorPaz-García, Marta
dc.contributor.authorRius, Cristina 
dc.contributor.authordel Monte, Alberto 
dc.contributor.authorRodriguez, Cristina
dc.contributor.authorFernández-García, Victoria
dc.contributor.authorAndres, Vicente 
dc.contributor.authorMartinez-Gonzalez, Jose
dc.contributor.authorLasunción, Miguel A
dc.contributor.authorMartín-Sanz, Paloma
dc.contributor.authorSoehnlein, Oliver
dc.contributor.authorBoscá, Lisardo
dc.date.accessioned2020-04-21T14:41:57Z
dc.date.available2020-04-21T14:41:57Z
dc.date.issued2019-03
dc.identifier.citationFASEB J. 2019; 33(3):3912-3921es_ES
dc.identifier.issn0892-6638es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/9669
dc.description.abstractAtherosclerosis is a chronic disease characterized by vascular lipid retention and inflammation, and pattern recognition receptors (PRRs) are important contributors in early stages of the disease. Given the implication of the intracellular PRR nucleotide-binding oligomerization domain 1 (NOD1) in cardiovascular diseases, we investigated its contribution to early atherosclerosis. We evidenced NOD1 induction in atherosclerotic human and mouse tissues, predominantly in vascular endothelial cells. Accordingly, NOD1 genetic inactivation in Apoe-/- mice reduced not only atherosclerosis burden, but also monocyte and neutrophil accumulation in atheromata. Of note, in the presence of either peptidoglycan or oxidized LDLs, endothelial NOD1 triggered VCAM-1 up-regulation through the RIP2-NF-κB axis in an autocrine manner, enhancing firm adhesion of both sets of myeloid cells to the inflamed micro- and macrovasculature in vivo. Our data define a major proatherogenic role for endothelial NOD1 in early leukocyte recruitment to the athero-prone vasculature, thus introducing NOD1 as an innovative therapeutic target and potential prognostic molecule.-González-Ramos, S., Paz-García, M., Rius, C., del Monte-Monge, A., Rodríguez, C., Fernández-García, V., Andrés, V., Martínez-González, J., Lasunción, M. A., Martín-Sanz, P., Soehnlein, O., Boscá, L. Endothelial NOD1 directs myeloid cell recruitment in atherosclerosis through VCAM-1.es_ES
dc.description.sponsorshipThis work was supported by the the Ministry of Science, Innovation and Universities (Grants SAF2015-64767-R, SAF2016-79490-R, SAF2015-70747-R, SAF2016-75004-R, SAF2017-82436-R/RTC2017-6283-1), the Center for Biomedical Research Network Consortium in Cardiovascular Diseases (Grants CB16/11/00257, CB16/11/00405, CB/11/00222), Community of Madrid Grant BMD/3686, the German Research Foundation (Grants SFB914 TP A02/B08/B09/Z03, SFB1123 TP A06/B05/B08/Z01), and the Netherlands Organization for Scientific Research (VIDI project 91712303). This project was also financed, in part, by the European Regional Development Fund. O.S. and L.B. contributed equally as senior authors. The authors declare no conflicts of interestes_ES
dc.language.isoenges_ES
dc.publisherFederation of American Societies for Experimental Biology (FASEB) es_ES
dc.type.hasVersionSMURes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectCardiovascular diseasees_ES
dc.subjectInnate immunityes_ES
dc.subjectLeukocytees_ES
dc.titleEndothelial NOD1 directs myeloid cell recruitment in atherosclerosis through VCAM-1es_ES
dc.typejournal articlees_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.identifier.pubmedID30496704es_ES
dc.format.volume33es_ES
dc.format.number3es_ES
dc.format.page3912-3921es_ES
dc.identifier.doi10.1096/fj.201801231RRes_ES
dc.contributor.funderMinisterio de Ciencia, Innovación y Universidades (España) 
dc.contributor.funderComunidad de Madrid (España) 
dc.contributor.funderDeutsche Forschungsgemeinschaft (Alemania) 
dc.contributor.funderDutch Research Council (Holanda) 
dc.contributor.funderUnión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) 
dc.identifier.e-issn1530-6860es_ES
dc.relation.publisherversionhttps://doi.org/10.1096/fj.201801231RRes_ES
dc.identifier.journalFASEB journal : official publication of the Federation of American Societies for Experimental Biologyes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Fisiopatología Cardiovascular Molecular y Genéticaes_ES
dc.repisalud.institucionCNICes_ES
dc.rights.accessRightsopen accesses_ES


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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
Este Item está sujeto a una licencia Creative Commons: Attribution-NonCommercial-NoDerivatives 4.0 Internacional