Repositorio de producción científica de la Universidad de Sevilla

miR-125a, miR-139 and miR-324 contribute to Urocortin protection against myocardial ischemia-reperfusion injury

 

Advanced Search
 

Show simple item record

dc.creator Díaz Carrasco, Ignacio es
dc.creator Calderón Sánchez, Eva María es
dc.creator Toro, Raquel del es
dc.creator Ávila Medina, Javier es
dc.creator Sánchez de Rojas de Pedro, Eva es
dc.creator Domínguez Rodríguez, Alejandro es
dc.creator Rosado, Juan Antonio es
dc.creator Hmadcha, Abdelkrim es
dc.date.accessioned 2017-09-14T09:57:20Z
dc.date.available 2017-09-14T09:57:20Z
dc.date.issued 2017
dc.identifier.citation Díaz Carrasco, I., Calderón Sánchez, E.M., Toro, R.d., Ávila Medina, J., Sánchez de Rojas de Pedro, E., Domínguez Rodríguez, A.,...,Hmadcha, A. (2017). miR-125a, miR-139 and miR-324 contribute to Urocortin protection against myocardial ischemia-reperfusion injury. Scientific Reports, 7 (8898)
dc.identifier.issn 2045-2322 es
dc.identifier.uri http://hdl.handle.net/11441/64425
dc.description.abstract Urocortin 1 and 2 (Ucn-1 and Ucn-2) have established protective actions against myocardial ischemia-reperfusion (I/R) injuries. However, little is known about their role in posttranscriptional regulation in the process of cardioprotection. Herein, we investigated whether microRNAs play a role in urocortin-induced cardioprotection. Administration of Ucn-1 and Ucn-2 at the beginning of reperfusion significantly restored cardiac function, as evidenced ex vivo in Langendorff-perfused rat hearts and in vivo in rat subjected to I/R. Experiments using microarray and qRT-PCR determined that the addition of Ucn-1 at reperfusion modulated the expression of several miRNAs with unknown role in cardiac protection. Ucn-1 enhanced the expression of miR-125a-3p, miR-324-3p; meanwhile it decreased miR-139-3p. Similarly, intravenous infusion of Ucn-2 in rat model of I/R mimicked the effect of Ucn-1 on miR-324-3p and miR-139-3p. The effect of Ucn-1 involves the activation of corticotropin-releasing factor receptor-2, Epac2 and ERK1/2. Moreover, the overexpression of miR-125a-3p, miR-324-3p and miR-139-3p promoted dysregulation of genes expression involved in cell death and apoptosis (BRCA1, BIM, STAT2), in cAMP and Ca2+ signaling (PDE4a, CASQ1), in cell stress (NFAT5, XBP1, MAP3K12) and in metabolism (CPT2, FoxO1, MTRF1, TAZ). Altogether, these data unveil a novel role of urocortin in myocardial protection, involving posttranscriptional regulation with miRNAs. es
dc.description.sponsorship España, Ministerio de Economía y Competitividad BFU2016-74932-C2; BFU2013-45564-C2 es
dc.description.sponsorship Junta de Andalucía P10-CVI-6095; P-12-CTS-1965; PI-0313-2016 es
dc.format application/pdf es
dc.language.iso eng es
dc.publisher Nature Publishing Group es
dc.relation.ispartof Scientific Reports, 7 (8898)
dc.rights Attribution-NonCommercial-NoDerivatives 4.0 Internacional *
dc.rights.uri http://creativecommons.org/licenses/by-nc-nd/4.0/ *
dc.title miR-125a, miR-139 and miR-324 contribute to Urocortin protection against myocardial ischemia-reperfusion injury es
dc.type info:eu-repo/semantics/article es
dc.type.version info:eu-repo/semantics/publishedVersion es
dc.rights.accessrights info:eu-repo/semantics/openAccess es
dc.relation.projectID info:eu-repo/grantAgreement/MINECO/BFU2016-74932-C2 es
dc.relation.projectID info:eu-repo/grantAgreement/MINECO/BFU2013-45564-C2 es
dc.relation.projectID P10-CVI-6095 es
dc.relation.projectID P-12-CTS-1965 es
dc.relation.projectID PI-0313-2016 es
dc.relation.publisherversion http://dx.doi.org10.1038/s41598-017-09198-x es
dc.identifier.doi /10.1038/s41598-017-09198-x es
idus.format.extent 12 p. es
dc.journaltitle Scientific Reports es
dc.publication.volumen 7 es
dc.publication.issue 8898 es
dc.contributor.funder Ministerio de Economía y Competitividad (MINECO). España
dc.contributor.funder Junta de Andalucía
Size: 2.482Mb
Format: PDF

This item appears in the following Collection(s)

Show simple item record