Arginase-2 Mediates Renal Ischemia/Reperfusion Injury.

Arginase-2 Mediates Renal Ischemia/Reperfusion Injury.
Am J Physiol Renal Physiol. 2017 May 17;:ajprenal.00620.2016
Authors: Raup-Konsavage WM, Gao T, Cooper TK, Morris SM, Reeves WB, Awad AS
Abstract
Novel therapeutic interventions for preventing or attenuating kidney injury following ischemia/reperfusion injury (IRI) remain a focus of significant interest. Currently, there are no definitive therapeutic or preventive approaches available for ischemic acute kidney injury (AKI). Our objective is to determine (a) whether renal arginase activity or expression is increased in renal IRI and (b) whether arginase plays a role in development of renal IRI. The impact of arginase activity and expression on renal damage was evaluated in male C57BL/6J (WT) and arginase-2 deficient (Arg2(-/-) ) mice subjected to bilateral renal ischemia for 28min followed by reperfusion for 24h. ARG2 expression and arginase activity significantly increased following renal IRI, paralleling the increase in kidney injury. Pharmacological blockade or genetic deficiency of Arg2 conferred kidney protection in renal IRI. Arg2(-/-) mice had significantly attenuated kidney injury and lower plasma creatinine and blood urea nitrogen levels after renal IRI. Blocking arginases using S-(2-boronoethyl)-L-cysteine (BEC) 18h before ischemia mimicked arginase deficiency by reducing kidney injury, histopathological changes and kidney injury marker-1 expression, renal apoptosis, kid...

Source: Am J Physiol Renal P... - May 17, 2017 Category: Urology & Nephrology Authors: Raup-Konsavage WM, Gao T, Cooper TK, Morris SM, Reeves WB, Awad AS Tags: Am J Physiol Renal Physiol Source Type: research