Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion.

摘要: Aims: Urocortin-2 (Ucn-2) is a potent cardioprotector against Ischemia and Reperfusion (I/R) injuries. However, little known about its role in the regulation of intracellular Ca2+ concentration ([Ca2+]i) under I/R. Here, we examined whether addition Ucn-2 reperfusion promotes cardioprotection focusing on ([Ca2+]i handling. Methods Results: Cardiac Wistar rat model I/R was induced by transient ligation left coronary artery experiments were conducted 1 week after surgery tissue adult cardiomyocytes isolated from risk remote zones. We observed that promoted significant alteration cardiac contractility as well an increase hypertrophy fibrosis both The study confocal [Ca2+]i imaging revealed decreased amplitude contraction Interestingly, intravenous infusion before heart’s recovered significantly prevented fibrosis, but it didn’t affect hypertrophy. Moreover, modulated expression several proteins related to homeostasis, such TRPC5 Orai1 channels. Using Neonatal Rat Ventricular Myocytes (NRVM) demonstrated blunted I/R-induced Store Operated Entry (SOCE), their interaction reperfusion. Conclusion: Our provides first evidences demonstrating at onset attenuates adverse remodeling, involving handling inhibiting between Orai1.