Surabhi Chandra

TL;DR: This study determined the mechanism involved in peroxynitrite and hydrogen peroxide‐induced enhancement in endothelial arginase activity and hypothesized that oxidative species increase argin enzyme activity through PKC‐activated RhoA/Rho kinase (ROCK) pathway.

TL;DR: Results indicate that ANG II increases endothelial arginase activity/expression through Gα12/13 G proteins coupled to AT(1) receptors and subsequent activation of RhoA/ROCK/p38 MAPK pathways leading to endothelial dysfunction.

TL;DR: Partial deletion of either ROCK isoform, but to a greater extent ROCK1, attenuates diabetes-induced vascular endothelial dysfunction by preventing increased arginase activity and expression and reduction in NO production in type 1 diabetes.

TL;DR: The present findings imply a direct role of ROS in PI induced deleterious effects on pancreatic β-cells and suggest that TQ may be used as a potential therapeutic agent to normalize the dysregulated insulin production observed in HAART treated patients.

TL;DR: The findings implicate a molecular mechanism of action of cocaine and a therapeutic effect of ETAR-specific inhibitor in suppressing the cocaine-induced endothelial dysfunction and suggest a concomitant increase in both ET-1 and ETAR expression in cocaine exposed HAECs may enhance signaling via the ETAR which decreases eNOS expression and NO production, and ultimately results in endothelial activation and leukocyte adhesion.