The Role of Cysteinyl-LT1Receptor (CysLT1R) in Renal Ischemia-Reperfusion Injury

Abstract The pathogenesis of ischemia-reperfusion (I/R) injury is known to involve cytokines and particularly surface adhesion molecules, the expression of which initiates the attachment of inflammatory cells. Renal I/R injury, a clinically important problem, is an invariable consequence of renal transplantation. The problem begins at the onset of acute tubular necrosis (ATN), when the transplantation includes a long ischemic interval or by use of a cardiac arrest donor's kidney. The cysteinyl leukotriene-1 (CysLT 1 ), a potent lipid mediator in allergic disease, acts through the CysLT 1 R receptor. We researched the expression of CysLT 1 R in rat renal I/R injury as well as correlations with the degree of ATN. The right kidney was harvested and the left renal artery and vein were clamped at laparotomy. The kidney was reperfused after 90 minutes of ischemia; rats were sacrificed at 0, 3, 5, 12, and 24 hours after reperfusion. CysLT 1 R expression was analyzed by immunohistochemistry. CysLT 1 R expression was observed only in endothelial cells of a normal kidney. CysLT 1 R expression was most intense on endothelial cells at 3 hours after reperfusion, and CysLT 1 R expression on endothelial cells gradually became weaker. Twelve hours after reperfusion, ATN extended throughout the ischemic kidney. Renal I/R injury gradually progressed at time after reperfusion. Several hours after the maximal CysLT 1 R expression, we observed the maximum renal I/R injury.