dc.creator | Domínguez Rodríguez, Alejandro | es |
dc.creator | Mayoral-González, Isabel | es |
dc.creator | Ávila Medina, Javier | es |
dc.creator | Sánchez de Rojas de Pedro, Eva | es |
dc.creator | Calderón Sánchez, Eva María | es |
dc.creator | Díaz Carrasco, Ignacio | es |
dc.creator | Hmadcha, Abdelkrim | es |
dc.creator | Castellano Orozco, Antonio Gonzalo | es |
dc.creator | Ordóñez Fernández, Antonio | es |
dc.creator | Smani Hajami, Tarik | es |
dc.date.accessioned | 2018-08-21T10:17:37Z | |
dc.date.available | 2018-08-21T10:17:37Z | |
dc.date.issued | 2018-07-03 | |
dc.identifier.citation | Domínguez Rodríguez, A., Mayoral-González, I., Ávila Medina, J., Sánchez de Rojas de Pedro, E., Calderón Sánchez, E.M., Díaz Carrasco, I.,...,Smani Hajami, T. (2018). Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion. Frontiers in Physiology, 9, 813-1-813-16. https://doi.org/10.3389/fphys.2018.00813. | |
dc.identifier.issn | 1664-042X | es |
dc.identifier.uri | https://hdl.handle.net/11441/78190 | |
dc.description.abstract | Aims: Urocortin-2 (Ucn-2) is a potent cardioprotector against Ischemia and Reperfusion (I/R) injuries. However, little is known about its role in the regulation of intracellular Ca2+ concentration ([Ca2+]i) under I/R. Here, we examined whether the addition of Ucn-2 in reperfusion promotes cardioprotection focusing on ([Ca2+]i handling.
Methods and Results: Cardiac Wistar rat model of I/R was induced by transient ligation of the left coronary artery and experiments were conducted 1 week after surgery in tissue and adult cardiomyocytes isolated from risk and remote zones. We observed that I/R promoted significant alteration in cardiac contractility as well as an increase in hypertrophy and fibrosis in both zones. The study of confocal [Ca2+]i imaging in adult cardiomyocytes revealed that I/R decreased the amplitude of [Ca2+]i transient and cardiomyocytes contraction in risk and remote zones. Interestingly, intravenous infusion of Ucn-2 before heart’s reperfusion recovered significantly cardiac contractility and prevented fibrosis, but it didn’t affect cardiac hypertrophy. Moreover, Ucn-2 recovered the amplitude of [Ca2+]i transient and modulated the expression of several proteins related to [Ca2+]i homeostasis, such as TRPC5 and Orai1 channels. Using Neonatal Rat Ventricular Myocytes (NRVM) we demonstrated that Ucn-2 blunted I/R-induced Store Operated Ca2+ Entry (SOCE), decreased the expression of TRPC5 and Orai1 as well as their interaction in reperfusion.
Conclusion: Our study provides the first evidences demonstrating that Ucn-2 addition at the onset of reperfusion attenuates I/R-induced adverse cardiac remodeling, involving the [Ca2+]i handling and inhibiting the expression and interaction between TRPC5 and Orai1. | es |
dc.description.sponsorship | FEDER funds No 316151 | es |
dc.description.sponsorship | Spanish Ministry of Economy and Competitiveness BFU2016-74932-C2 BFU2013-45564-C2 | es |
dc.description.sponsorship | Institute of Carlos III PI15/00203 PI16/00259 CB16/11/00431 | es |
dc.description.sponsorship | Andalusia Government P12-CTS-1965 PI-0313-2016 PI-0108-2012 P12-CTS-1965 PI-0313-2016 | es |
dc.description.sponsorship | Agence Nationale de la Recherche ANR-13-BSVI-0023-01 | es |
dc.format | application/pdf | es |
dc.language.iso | eng | es |
dc.publisher | Frontiers Research Foundation | es |
dc.relation.ispartof | Frontiers in Physiology, 9, 813-1-813-16. | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | Urocortin-2 | es |
dc.subject | Ischemia and reperfusion | es |
dc.subject | Adverse remodeling | es |
dc.subject | Ca2+ dysregulation | es |
dc.subject | Store operated Ca2+ channels | es |
dc.title | Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion | 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 | Instituto de Biomedicina de Sevilla (IBIS) | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica | es |
dc.contributor.affiliation | Centro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER) | es |
dc.relation.projectID | 316151 | es |
dc.relation.projectID | BFU2016-74932-C2 | es |
dc.relation.projectID | BFU2013-45564-C2 | es |
dc.relation.projectID | PI15/00203 | es |
dc.relation.projectID | PI16/00259 | es |
dc.relation.projectID | CB16/11/00431 | es |
dc.relation.projectID | P12-CTS-1965 | es |
dc.relation.projectID | PI-0313-2016 | es |
dc.relation.projectID | PI-0108-2012 | es |
dc.relation.projectID | P12-CTS-1965 | es |
dc.relation.projectID | PI-0313-2016 | es |
dc.relation.projectID | ANR-13-BSVI-0023-01 | es |
dc.relation.publisherversion | https://doi.org/10.3389/fphys.2018.00813 | es |
dc.identifier.doi | 10.3389/fphys.2018.00813 | es |
idus.format.extent | 16 p. | es |
dc.journaltitle | Frontiers in Physiology | es |
dc.publication.volumen | 9 | es |
dc.publication.initialPage | 813-1 | es |
dc.publication.endPage | 813-16 | es |
dc.description.awardwinning | Premio Anual Publicación Científica Destacada de la US. Facultad de Medicina | |