dc.creator | Mayoral-González, Isabel | es |
dc.creator | Calderón Sánchez, Eva M. | es |
dc.creator | Galeano-Otero, Isabel | es |
dc.creator | Martín Bórnez, Marta | es |
dc.creator | Gutiérrez Carretero, Encarnación | es |
dc.creator | Fernández Velasco, María | es |
dc.creator | Ordóñez Fernández, José Antonio | es |
dc.creator | Smani Hajami, Tarik | es |
dc.date.accessioned | 2022-12-01T14:39:30Z | |
dc.date.available | 2022-12-01T14:39:30Z | |
dc.date.issued | 2022 | |
dc.identifier.citation | Mayoral-González, I., Calderón Sánchez, E.M., Galeano-Otero, I., Martín Bórnez, M., Gutiérrez Carretero, E., Fernández Velasco, M.,...,Smani Hajami, T. (2022). Cardiac protection induced by urocortin-2 enables the regulation of apoptosis and fibrosis after ischemia and reperfusion involving miR-29a modulation. Molecular Therapy-Nucleic Acids, 27, 838-853. https://doi.org/10.1016/j.omtn.2022.01.003. | |
dc.identifier.issn | 2162-2531 | es |
dc.identifier.uri | https://hdl.handle.net/11441/140032 | |
dc.description.abstract | Urocortin-2 (Ucn-2) has demonstrated cardioprotective ac tions against myocardial ischemia-reperfusion (I/R) injuries.
Herein, we explored the protective role of Ucn-2 through
microRNAs (miRNAs) post-transcriptional regulation of
apoptotic and pro-fibrotic genes. We determined that the
intravenous administration of Ucn-2 before heart reperfusion
in a Wistar rat model of I/R recovered cardiac contractility
and decreased fibrosis, lactate dehydrogenase release, and
apoptosis. The infusion of Ucn-2 also inhibited the upregula tion of 6 miRNAs in revascularized heart. The in silico analysis
indicated that miR-29a and miR-451_1* are predicted to
target many apoptotic and fibrotic genes. Accordingly, the
transfection of neonatal rat ventricular myocytes with mimics
overexpressing miR-29a, but not miR-451_1*, prevented I/R induced expression of pro- and anti-apoptotic genes such as
Apaf-1, Hmox-1, and Cycs, as well as pro-fibrotic genes Col-I
and Col-III. We also confirmed that Hmox-1, target of miR 29a, is highly expressed at the mRNA and protein levels in
adult rat heart under I/R, whereas, Ucn-2 abolished I/R induced mRNA and protein upregulation of HMOX-1. Inter estingly, a significant upregulation of Hmox-1 was observed in
the ventricle of ischemic patients with heart failure, corre lating negatively with the left ventricle ejection fraction.
Altogether, these data indicate that Ucn-2, through miR-29a
regulation, provides long-lasting cardioprotection, involving
the post-transcriptional regulation of apoptotic and fibrotic
genes. | es |
dc.format | application/pdf | es |
dc.format.extent | 16 p. | es |
dc.language.iso | eng | es |
dc.publisher | CELL PRESS (Elsevier) | es |
dc.relation.ispartof | Molecular Therapy-Nucleic Acids, 27, 838-853. | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | Cardiac protection induced | es |
dc.subject | Urocortin-2 | es |
dc.subject | Apoptosis | es |
dc.subject | Fibrosis | es |
dc.subject | Ischemia | es |
dc.title | Cardiac protection induced by urocortin-2 enables the regulation of apoptosis and fibrosis after ischemia and reperfusion involving miR-29a modulation | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Cirugía | es |
dc.relation.publisherversion | https://www.sciencedirect.com/science/article/pii/S2162253122000087?via%3Dihub | es |
dc.identifier.doi | 10.1016/j.omtn.2022.01.003 | es |
dc.journaltitle | Molecular Therapy-Nucleic Acids | es |
dc.publication.volumen | 27 | es |
dc.publication.initialPage | 838 | es |
dc.publication.endPage | 853 | es |
dc.description.awardwinning | Premio Mensual Publicación Científica Destacada de la US. Facultad de Medicina | |