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dc.contributor.authorCuadrado Berrocal, Irene 
dc.contributor.authorCastejón, Borja
dc.contributor.authorMartín, Ana María
dc.contributor.authorSaura Redondo, Marta 
dc.contributor.authorReventun Torralba, Paula 
dc.contributor.authorZamorano Gómez, José Luís 
dc.contributor.authorZaragoza Sánchez, Carlos 
dc.date.accessioned2018-07-10T13:56:30Z
dc.date.available2018-07-10T13:56:30Z
dc.date.issued2016-09-20
dc.identifier.bibliographicCitationPLoS ONE, 2016, v. 11, n. 9, p. e0162912en
dc.identifier.urihttp://hdl.handle.net/10017/33764
dc.description.abstractInhibition of Extracellular Matrix degradation by nitric oxide (NO) induces cardiac protection against coronary ischemia/reperfusion (IR). Glycosylation of Extracellular Matrix Metalloproteinase Inducer (EMMPRIN) stimulates enzymatic activation of matrix metalloproteinases (MMPs) in the heart, although the mechanisms leading to EMMPRIN glycosylation are poorly understood. We sought to determine if NO may induce cardiac protection by preventing glycosylation of EMMPRIN in a mouse model of IR. Here we found that Caveolin-3 binds to low glycosylated EMMPRIN (LG-EMMPRIN) in cardiac cells and in the hearts of healthy mice, whereas IR disrupted the complex in nitric oxide synthase 2 (NOS2) knockout (KO) mice. By contrast, the binding was partially restored when mice were fed with an NO donor (DEA-NO) in the drinking water, showing a significant reduction on infarct size (NOS2KO: 34.6±5 vs NOS2KO+DEA-NO: 20.7±9), in expression of matrix metalloproteinases, and cardiac performance was improved (left ventricular ejection fraction (LVEF). NOS2KO: 31±4 vs NOS2KO+DEA-NO: 46±6). The role of Caveolin-3/EMMPRIN in NO-mediated cardiac protection was further assayed in Caveolin-3 KO mice, showing no significant improvement on infarct size (Caveolin-3 KO: 34.8±3 vs Caveolin-3 KO+DEA-NO:33.7±5), or in the expression of MMPs, suggesting that stabilization of the complex Caveolin-3/LG-EMMPRIN may play a significant role in the cardioprotective effect of NO against IR.en
dc.description.sponsorshipMinisterio de Economía y Competitividades_ES
dc.description.sponsorshipInstituto de Salud Carlos IIIes_ES
dc.format.mimetypeapplication/pdfen
dc.language.isoenges
dc.publisherUtpal Sen, University of Louisville, UNITED STATESen
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacionalen
dc.rights(c) Cuadrado et al., 2016es-ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en
dc.subjectExtracellular Matrixen
dc.subjectMyocardial Reperfusion Injuryen
dc.subjectMyocytes, Cardiacen
dc.subjectNitric Oxideen
dc.subjectProtective Agentsen
dc.titleNitric Oxide Induces Cardiac Protection by Preventing Extracellular Matrix Degradation through the Complex Caveolin-3/EMMPRIN in Cardiac Myocytes.en
dc.typeinfo:eu-repo/semantics/articleen
dc.subject.ecienciaFisiologíaes_ES
dc.subject.ecienciaPhysiologyen
dc.contributor.affiliationUniversidad de Alcalá. Departamento de Biología de Sistemases_ES
dc.type.versioninfo:eu-repo/semantics/publishedVersionen
dc.identifier.doi10.1371/journal.pone.0162912
dc.relation.projectIDinfo:eu-repo/grantAgreement/ISCIII//PI14%2F02022/ES/Inhibición de la degradación de la matriz extracelular como herramienta preventiva frente al ictus isquémico de origen aterosclerótico y su evaluación mediante imagen molecular no invasivaes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/MINECO//SAF2012-35141/ES/CONTRIBUCIÓN DE LA QUINASA LIGADA A INTEGRINAS (ILK) A LA REGULACIÓN DEL SISTEMA DEL NO Y LA VÍA UB-PROTEASOMA EN LA REMODELACIÓN VASCULAR ASOCIADA A ATEROESCLEROSISes_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessen
dc.identifier.publicationtitlePloS oneen
dc.identifier.publicationvolume11
dc.identifier.publicationissue9
dc.identifier.publicationfirstpagee0162912
dc.identifier.pmid27649573
dc.subject.meshAnimalsen
dc.subject.meshBasiginen
dc.subject.meshCaveolin 3en
dc.subject.meshCell Lineen
dc.subject.meshExtracellular Matrixen
dc.subject.meshGlycosylationen
dc.subject.meshHydrazinesen
dc.subject.meshImmunoblottingen
dc.subject.meshMiceen
dc.subject.meshMice, Knockouten
dc.subject.meshMicroscopy, Confocalen
dc.subject.meshMultiprotein Complexesen
dc.subject.meshMyocardial Infarctionen
dc.subject.meshMyocardial Reperfusion Injuryen
dc.subject.meshMyocytes, Cardiacen
dc.subject.meshNitric Oxideen
dc.subject.meshNitric Oxide Donorsen
dc.subject.meshNitric Oxide Synthase Type IIen
dc.subject.meshProtective Agentsen
dc.identifier.essn1932-6203


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