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dc.contributor.authorVarga, Zoltán V
dc.contributor.authorPipicz, Márton
dc.contributor.authorBaán, Júlia A
dc.contributor.authorBaranyai, Tamás
dc.contributor.authorKoncsos, Gábor
dc.contributor.authorLeszek, Przemyslaw
dc.contributor.authorKuśmierczyk, Mariusz
dc.contributor.authorSanchez-Cabo, Fatima 
dc.contributor.authorGarcía-Pavía, Pablo
dc.contributor.authorBrenner, Gábor J
dc.contributor.authorGiricz, Zoltán
dc.contributor.authorCsont, Tamás
dc.contributor.authorMendler, Luca
dc.contributor.authorLara-Pezzi, Enrique 
dc.contributor.authorPacher, Pál
dc.contributor.authorFerdinandy, Péter
dc.date.accessioned2019-02-21T11:34:35Z
dc.date.available2019-02-21T11:34:35Z
dc.date.issued2017
dc.identifier.citationFront Physiol. 2017; 8:935es_ES
dc.identifier.issn1664-042Xes_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7208
dc.description.abstractIncreased oxidative stress is a major contributor to the development and progression of heart failure, however, our knowledge on the role of the distinct NADPH oxidase (NOX) isoenzymes, especially on NOX4 is controversial. Therefore, we aimed to characterize NOX4 expression in human samples from healthy and failing hearts. Explanted human heart samples (left and right ventricular, and septal regions) were obtained from patients suffering from heart failure of ischemic or dilated origin. Control samples were obtained from donor hearts that were not used for transplantation. Deep RNA sequencing of the cardiac transcriptome indicated extensive alternative splicing of the NOX4 gene in heart failure as compared to samples from healthy donor hearts. Long distance PCR analysis with a universal 5'-3' end primer pair, allowing amplification of different splice variants, confirmed the presence of the splice variants. To assess translation of the alternatively spliced transcripts we determined protein expression of NOX4 by using a specific antibody recognizing a conserved region in all variants. Western blot analysis showed up-regulation of the full-length NOX4 in ischemic cardiomyopathy samples and confirmed presence of shorter isoforms both in control and failing samples with disease-associated expression pattern. We describe here for the first time that NOX4 undergoes extensive alternative splicing in human hearts which gives rise to the expression of different enzyme isoforms. The full length NOX4 is significantly upregulated in ischemic cardiomyopathy suggesting a role for NOX4 in ROS production during heart failure.es_ES
dc.description.sponsorshipThe study was supported by the grants from the Hungarian Scientific Research Fund (OTKA ANN107803, OTKA K109737 to PF) by the National Research, Development and Innovation Fund of Hungary (Project no. NVKP_16-1-2016-0017 has been implemented with the support provided from the National Research, Development and Innovation Fund of Hungary, financed under the NVKP_16 funding scheme). ZVV was supported by the National Program of Excellence (TAMOP 4.2.4.A/1-11-1-2012-0001) and by the Rosztoczy Foundation. PF was a Szentagothai Fellow of the National Program ofExcellence (TAMOP 4.2.4.A/2-11-1-2012-0001). ZG held a “János Bolyai Fellowship” from the Hungarian Academy of Sciences (awarded in 2013 and 2017). TB is supported by the UNKP-16-3 New National Excellence Program of The Ministry of Human Capacities. PP is supported by the Intramural Research Program of NIAAA. PF is a vice chair, PL and ZG are management committee members of the EU-Cardioprotection COST Action CA16225.es_ES
dc.language.isoenges_ES
dc.publisherFrontiers in Biosciencees_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectaginges_ES
dc.subjectcardiac dysfunctiones_ES
dc.subjectcardiomyopathyes_ES
dc.subjectmyocardiumes_ES
dc.subjectoxidative stresses_ES
dc.titleAlternative Splicing of NOX4 in the Failing Human Heartes_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID29204124es_ES
dc.format.volume8es_ES
dc.format.page935es_ES
dc.identifier.doi10.3389/fphys.2017.00935es_ES
dc.contributor.funderHungarian Scientific Research Fundes_ES
dc.contributor.funderRosztoczy Foundationes_ES
dc.contributor.funderHungarian Academy of Scienceses_ES
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.3389/fphys.2017.00935es_ES
dc.identifier.journalFrontiers in physiologyes_ES
dc.repisalud.orgCNICCNIC::Unidades técnicas::Bioinformáticaes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Regulación Molecular de la Insuficiencia Cardiacaes_ES
dc.repisalud.institucionCNICes_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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