Activation of the CaR-CSE/H2S pathway confers cardioprotection against ischemia-reperfusion injury.

Activation of the CaR-CSE/H2S pathway confers cardioprotection against ischemia-reperfusion injury. Exp Cell Res. 2020 Nov 19;:112389 Authors: Luo Y, Liu LM, Xie L, Zhao HL, Lu YK, Wu BQ, Wu ZY, Zhang ZL, Hao YL, Ou WH, Liu RS, Xu WM, Chen XH Abstract Ischemia-reperfusion (I/R) injury is a multifactorial process triggered when an organ is subjected to transiently reduced blood supply. The result is a cascade of pathological complications and organ damage due to the production of reactive oxygen species following reperfusion. The present study aims to evaluate the role of activated calcium-sensing receptor (CaR)-cystathionine γ-lyase (CSE)/hydrogen sulfide (H2S) pathway in I/R injury. Firstly, an I/R rat model with CSE knockout was constructed. Transthoracic echocardiography, TTC and HE staining were performed to determine the cardiac function of rats following I/R Injury, followed by TUNEL staining observation on apoptosis. Besides, with the attempt to better elucidate how CaR-CSE/H2S affects I/R, in-vitro culture of human coronary artery endothelial cells (HCAECs) was conducted with gadolinium chloride (GdCl3, a CaR agonist), H2O2, siRNA against CSE (siCSE), or W7 (a CaM inhibitor). The interaction between CSE and CaM was subsequently detected. Plasma oxidative stress indexes, H2S and CSE, and apoptosis-related proteins were all analyzed following cell apoptosis. We found that H2S elevation led to the improvement whereas CSE knockd...
Source: Experimental Cell Research - Category: Cytology Authors: Tags: Exp Cell Res Source Type: research