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dc.contributor.authorRamirez-Carracedo, Rafael
dc.contributor.authorTesoro, Laura
dc.contributor.authorHernandez, Ignacio
dc.contributor.authorDiez-Mata, Javier
dc.contributor.authorFilice, Marco 
dc.contributor.authorToro, Rocio
dc.contributor.authorRodriguez-Pinero, Manuel
dc.contributor.authorLuis Zamorano, Jose
dc.contributor.authorSaura, Marta
dc.contributor.authorZaragoza, Carlos 
dc.date.accessioned2018-11-22T08:10:50Z
dc.date.available2018-11-22T08:10:50Z
dc.date.issued2018
dc.identifierISI:000448951000403
dc.identifier.citationInt J Mol Sci. 2018; 19(10):E3248
dc.identifier.issn1422-0067
dc.identifier.urihttp://hdl.handle.net/20.500.12105/6663
dc.description.abstractLack of endothelial nitric oxide causes endothelial dysfunction and circulating monocyte infiltration, contributing to systemic atheroma plaque formation in arterial territories. Among the different inflammatory products, macrophage-derived foam cells and smooth muscle cells synthesize matrix metalloproteinases (MMPs), playing a pivotal role in early plaque formation and enlargement. We found increased levels of MMP-9 and MMP-13 in human endarterectomies with advanced atherosclerosis, together with significant amounts of extracellular matrix (ECM) metalloproteinase inducer EMMPRIN. To test whether the absence of NO may aggravate atherosclerosis through EMMPRIN activation, double NOS3/apoE knockout (KO) mice expressed high levels of EMMPRIN in carotid plaques, suggesting that targeting extracellular matrix degradation may represent a new mechanism by which endothelial NO prevents atherosclerosis. Based on our previous experience, by using gadolinium-enriched paramagnetic fluorescence micellar nanoparticles conjugated with AP9 (NAP9), an EMMPRIN-specific binding peptide, magnetic resonance sequences allowed non-invasive visualization of carotid EMMPRIN in NOS3/apoE over apoE control mice, in which atheroma plaques were significantly reduced. Taken together, these results point to EMMPRIN as a new therapeutic target of NO-mediated protection against atherosclerosis, and NAP9 as a non-invasive molecular tool to target atherosclerosis.
dc.description.sponsorshipThis research was funded by (CZ) ``Instituto de Salud Carlos III, PI14/02022 (Plan Estatal de I+ D+ i 2013-2016) co-financed by the European Development Regional Fund A way to achieve Europe (ERDF)´´ and ``Universidad Francisco de Vitoria 2014, 2015, and 2016´´. (MF) ``Comunidad Autonoma de Madrid 2017-T1/BIO-4992. Atraccion de Talento´´ and ``Universidad Complutense de Madrid and the I + D collaborative Programme in Biomedicine NIETO-CM (B2017-BMD3731)´´.
dc.language.isoeng
dc.publisherMultidisciplinary Digital Publishing Institute (MDPI) 
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectNitric oxide
dc.subjectEndothelial nitric oxide synthase
dc.subjectMetalloproteinsases
dc.subjectNanoparticles
dc.subjectMagnetic resonance imaging
dc.subjectExtacellular matrix metalloproteinase inducer EMMPRIN
dc.subjectCELL-SURFACE EXPRESSION
dc.subjectIN-VIVO
dc.subjectLIGAND CYCLOPHILIN
dc.subjectCD147
dc.subjectMMP-9
dc.subjectCD147/EMMPRIN
dc.subjectCAVEOLIN-1
dc.subjectADHESION
dc.subjectDISEASE
dc.subjectMICE
dc.titleNon-Invasive Detection of Extracellular Matrix Metalloproteinase Inducer EMMPRIN, a New Therapeutic Target against Atherosclerosis, Inhibited by Endothelial Nitric Oxide
dc.typejournal article
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID30347750
dc.format.volume19
dc.identifier.doi10.3390/ijms19103248
dc.contributor.funderInstituto de Salud Carlos III 
dc.contributor.funderComunidad de Madrid (España) 
dc.contributor.funderComplutense University of Madrid (España) 
dc.contributor.funderFrancisco de Vitoria University (España) 
dc.contributor.funderUnión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) 
dc.description.peerreviewed
dc.relation.publisherversionhttps://doi.org/10.3390/ijms19103248
dc.identifier.journalINTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
dc.repisalud.orgCNICCNIC::Unidades técnicas
dc.repisalud.institucionCNIC
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI14/02022es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/2017-T1/BIO-4992es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/B2017-BMD3731es_ES
dc.rights.accessRightsopen accesses_ES


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