XPO1 gene therapy attenuates cardiac dysfunction in rats with chronic induced myocardial infarction

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dc.centroUniversidad Cardenal Herrera-CEU
dc.contributor.authorTarazón Melguizo, Estefanía
dc.contributor.authorOrtega, Ana
dc.contributor.authorGil Cayuela, Carolina
dc.contributor.authorMartínez Dolz, Luis
dc.contributor.authorGonzález Juanatey, José Ramón
dc.contributor.authorLago Paz, Francisca
dc.contributor.authorPortolés Sanz, Manuel
dc.contributor.authorRoselló Lletí, Esther
dc.contributor.authorRivera Otero, Miguel
dc.contributor.authorGarcía Manzanares, María Dolores
dc.contributor.otherProducción Científica UCH 2020
dc.contributor.otherUCH. Departamento de Medicina y Cirugía Animal
dc.contributor.otherUCH. Departamento de Producción y Sanidad Animal, Salud Pública Veterinaria y Ciencia y Tecnología de los Alimentos
dc.date2020
dc.date.accessioned2020-06-17T04:00:16Z
dc.date.available2020-06-17T04:00:16Z
dc.date.issued2020-08-01
dc.descriptionEste es el artículo que se ha publicado de forma definitiva en: https://link.springer.com/article/10.1007/s12265-019-09932-y
dc.description.abstractTranscriptomic signature ofXPO1was highly expressed and inversely related to left ventricular function in ischemic cardiomy-opathy patients. We hypothesized that treatment with AAV9-shXPO1 attenuates left ventricular dysfunction and remodeling in amyocardial infarction rat model. We induced myocardial infarction by coronary ligation in Sprague-Dawley rats (n= 10), whichreceived AAV9-shXPO1 (n= 5) or placebo AAV9-scramble (n= 5) treatment. Serial echocardiographic assessment was per-formed throughout the study. After myocardial infarction, AAV9-shXPO1-treated rats showed partial recovery of left ventricularfractional shortening (16.8 ± 2.8 vs 24.6 ± 4.1%,P< 0.05) and a maintained left ventricular dimension (6.17 ± 0.95 vs 4.70 ±0.93 mm,P< 0.05), which was not observed in non-treated rats. Furthermore, lower levels of EXP-1 (P< 0.05) and lowercollagen fibers and fibrosis in cardiac tissue were observed. However, no differences were found in the IL-6 or TNFR1 plasmalevels of the myocardium of AAV9-shXPO1 rats. AAV9-shXPO1 administration attenuates cardiac dysfunction and remodelingin rats after myocardial infarction, producing the gene silencing ofXPO1.
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dc.identifier.citationGarcía-Manzanares, M., Tarazón, E., Ortega, A., Gil-Cayuela, C., Martínez-Dolz, L., González-Juanatey, JR. et al. (2019). XPO1 gene therapy attenuates cardiac dysfunction in rats with chronic induced myocardial infarction. Journal of Cardiovascular Translational Research, vol. 13, i. 4 (01 aug.), pp. 593-600. DOI: https://doi.org/10.1007/s12265-019-09932-y
dc.identifier.doihttps://doi.org/10.1007/s12265-019-09932-y
dc.identifier.issn1937-5387.
dc.identifier.issn1937-5395 (Electrónico).
dc.identifier.urihttp://hdl.handle.net/10637/10854
dc.language.isoen
dc.language.isoes
dc.publisherSpringer Nature.
dc.relationEste trabajo ha sido financiado por el Instituto Nacional de Salud "Fondo de Investigaciones Sanitarias del Instituto de Salud CarlosIII" [PI16/01627, PI17/01925, PI17/01232], el "Consorcio Centro de Investigación Biomédica en Red, M.P."[CIBERCV, bajo la beca CB16/11/00261] y el Fondo Europeo de Desarrollo Regional (FEDER).
dc.relationUCH. Financiación Nacional
dc.relationUCH. Financiación Europea.
dc.relation.ispartofJournal of Cardiovascular Translational Research, vol. 13, n. 4.
dc.relation.projectIDPI16/01627
dc.relation.projectIDPI17/01925
dc.relation.projectIDPI17/01232
dc.relation.projectIDCB16/11/00261
dc.rightsopen access
dc.rights.cchttps://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
dc.subjectHeart - Ventricles - Diseases - Treatment.
dc.subjectInfarto de miocardio - Tratamiento.
dc.subjectEukaryotic cells.
dc.subjectCorazón - Ventrículos - Enfermedades - Tratamiento.
dc.subjectMyocardial infarction - Treatment.
dc.subjectCélulas eucariotas.
dc.titleXPO1 gene therapy attenuates cardiac dysfunction in rats with chronic induced myocardial infarction
dc.typeArtículo
dspace.entity.typePublicationes
relation.isAuthorOfPublicatione7a20087-ccfb-4f1a-9919-87100855bd84
relation.isAuthorOfPublication.latestForDiscoverye7a20087-ccfb-4f1a-9919-87100855bd84

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