Study of Cysteinyl Leukotriene-1 Receptor in Rat Renal Ischemia-Reperfusion Injury

• Published in: Transplantation proceedings 2008-09, Vol.40 (7), p.2149-2151
• Main Authors: Matsuyama, M, Funao, K, Kawahito, Y, Sano, H, Chargui, J, Touraine, J.-L, Takemoto, Y, Nakatani, T, Yoshimura, R
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Immunohistochemistry; Kidney - metabolism; Kidney - pathology; Kidney Tubular Necrosis, Acute - metabolism; Kidney Tubular Necrosis, Acute - pathology; Male; Medical sciences; Nephrology. Urinary tract diseases; Nephropathies. Renovascular diseases. Renal failure; Rats; Rats, Inbred Lew; Receptors, Leukotriene - metabolism; Renal Circulation; Renovascular diseases; Reperfusion Injury - metabolism; Surgery; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases; Tissue, organ and graft immunology
• ISSN: 0041-1345; 1873-2623
• DOI: 10.1016/j.transproceed.2008.06.009

Abstract Renal ischemia-reperfusion (I/R) injury is a major cause of renal transplant dysfunction. Recent studies of I/R injury have focused on the function of neutrophils, the mechanisms of action of inflammatory cytokines, and oxygen free radicals, as well as other mediators. However, few reports address the cysteinyl leukotriene-1 receptor (CysLT1 R), an important mediator of bronchial asthma in human beings. We examined the expression of CysLT1 R in rat renal I/R injury. At laparotomy, the right kidney was harvested and the left renal artery and vein were clamped. The kidney was reperfused after 90 minutes of ischemia, and the rats were killed after 0, 3, 5, 12, or 24 hours. Expression of CysLT1 R analyzed at immunohistochemistry was observed only in endothelial cells in nonischemic kidney. At 0 to 3 hours after reperfusion, CysLT1 R expression on endothelial cells gradually became stronger, being most intense at 3 hours after reperfusion. Twelve hours after reperfusion, necrosis extended throughout the ischemic kidney; nearly all of the tubular epithelial cells were destroyed. At 3 to 12 hours after reperfusion, CysLT1 R expression gradually became weaker on endothelial cells. At 24 hours after reperfusion, CysLT1 R expression was almost at the level of that in nonischemic kidney. Expression of CysLT1 R was noted in a rat model of renal I/R injury. Several hours after the maximal CysLT1 R expression, we observed the maximum renal I/R injury. These results may suggest a relationship between the CysLT1 R and renal I/R injury.