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dc.contributor.authorDíaz del Moral, Sandra
dc.contributor.authorWagner, Kay
dc.contributor.authorWagner, Nicole
dc.contributor.authorBenaouicha, Maha
dc.contributor.authorMuñoz-Chápuli-Oriol, Ramón 
dc.contributor.authorCarmona-Mejías, Rita María 
dc.date.accessioned2022-05-18T06:59:37Z
dc.date.available2022-05-18T06:59:37Z
dc.date.created2022
dc.date.issued2022-05
dc.identifier.urihttps://hdl.handle.net/10630/24142
dc.descriptionEstudio de la deleción del gen supresor del Tumor de Wilms en cardiomiocitos adultos en un modelo de ratón.es_ES
dc.description.abstractThe Wilms tumor suppressor gene (Wt1) encodes a C2H2-type zinc-finger transcription factor that participates in transcriptional regulation, RNA metabolism and protein-protein interactions. WT1 is critically involved in the development of several organs, including kidneys and gonads, spleen, adrenals, liver, and diaphragm (Hastie, 2017). WT1 is highly expressed in the embryonic epicardium where it regulates a process of epicardial-mesenchymal transformation and the development of the epicardial-derived cells. We have recently shown evidence of a transient Wt1 expression in about 25% of cardiomyocytes of mouse embryos. Conditional deletion of this expression in the cardiac troponin T lineage caused abnormal sinus venosus and atrium development, thin ventricular myocardium and, in some cases, interventricular septum and cardiac wall defects (Díaz del Moral et al., Front Cell Dev Biol. 2021;9:683861). We aimed to know if Wt1 is also expressed in adult cardiomyocytes and what could be the consequences of its conditional deletion for cardiac homeostasis and/or in the response to damage induced by isoproterenol and doxorubicin treatments. For conditional deletion of Wt1 in cardiomyocytes, we generated tamoxifen inducible Wt1 mutants by crossing MHCMerCreMer mice with homozygous Wt1 conditional mice, where the first exon of Wt1 is flanked by loxP sites. We have found experimental evidence of a low expression of Wt1 in postnatal murine cardiomyocytes, using reporter and lineage tracing models as well as qPCR. Our preliminary data suggest that conditional deletion of Wt1 in cardiomyocytes induces interstitial fibrosis, increased oxidative stress markers, altered metabolism and mitochondrial dysfunction in Wt1-deficient cardiomyocytes. In addition, conditional deletion of Wt1 in adult cardiomyocytes increases the damage induced by doxorubicin and isoproterenol treatments. These findings suggest a novel role of Wt1 in myocardial physiology and protection against damage.es_ES
dc.description.sponsorshipUniversidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.es_ES
dc.language.isoenges_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectNefroblastomaes_ES
dc.subjectEstrés oxidativoes_ES
dc.subject.otherWilms tumor suppressor genees_ES
dc.subject.otherMyocardiumes_ES
dc.subject.otherOxidative stresses_ES
dc.titleThe Wilms’ tumor suppressor gene is expressed in adult cardiomyocytes and it regulates myocardial metabolism and response to damagees_ES
dc.typeinfo:eu-repo/semantics/conferenceObjectes_ES
dc.centroFacultad de Medicinaes_ES
dc.relation.eventtitleWeinstein Conference, 2022es_ES
dc.relation.eventplaceMarsella (Francia)es_ES
dc.relation.eventdateDel 12 al 14 de mayor de 2022es_ES
dc.rights.ccAttribution-NonCommercial-NoDerivatives 4.0 Internacional*


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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
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