ICMT role in the response to renal ischemic damage

BORINI ETICHETTI CARLA; FUSSI M. FERNANDA; MONASTEROLO, LILIANA A.; LAROCCA, M. CECILIA; MOLINAS, SARA M.; GIRARDINI JAVIER

Mar del Plata

Congreso; Reunión Anual de Sociedades de Biociencias SAIC, SAFIS, SAI 2022; 2022

Sociedad Argentina de Investigación Clínica y Sociedad Argentina de Fisiología

Renal ischemia-reperfusion (IR) is one of the main causes of acutekidney injury (AKI). Rho GTPases, RhoA and Cdc42, act as regulatorsof various processes that directly impact the ability of the renalepithelium to regenerate. A key regulator of these Rho GTPasesis the enzyme Isoprenyl-cysteine carboxymethyltransferase (ICMT),which participates in the post- translational modification of theirC-terminus.The aim of this work was to investigate the role of ICMTin the epithelial tubular cell response to ischemic AKI. We previouslydemonstrated that, in IR rats, the early stage of renal damage is associatedwith a decrease in RhoA, Cdc42 and ICMT and the stage ofmarked regeneration is associated with an increment of these proteins.We also demonstrated that Angiotensin II type 2 receptor activation by its agonist, C21, prevented renal IR tubular epithelial cell damage in rats. Here, we found that C21 (1 mg/kg/day, i.p.) preventedthe decrease in ICMT abundance in Wistar rats submitted to 40min unilateral renal ischemia + 1 day of reperfusion (-55%, p