Expression of Fas Ligand (FasL) in Normal Kidney and Experimental Acute Tubular Necrosis.
- Author:
Wan Seop KIM
1
;
Jung Woo NOH
;
Moon Hyang PARK
Author Information
1. Department of Pathology, College of Medicine, Hanyang University, Seoul, Korea. parkmh@hanyang.ac.kr
- Publication Type:Original Article
- Keywords:
Kidney;
Acute tubular necrosis;
Fas ligand;
Rhabdomyolysis;
Apoptosis
- MeSH:
Acute Kidney Injury;
Antigens, CD95;
Apoptosis;
Cell Proliferation;
Epithelial Cells;
Fas Ligand Protein*;
Glycerol;
Hemorrhage;
Immunohistochemistry;
In Situ Nick-End Labeling;
Kidney*;
Necrosis*;
Rabbits;
Rhabdomyolysis
- From:Korean Journal of Nephrology
2005;24(3):358-365
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Fas ligand (FasL) is a lethal cytokine that promotes apoptosis through activation of the Fas receptor. There are few studies on the expression of FasL in normal or injured renal tissue. We have shown previously that apoptotic cells were identified by TUNEL and tissue-transglutaminase staining in the tubular cells of experimental acute tubular necrosis model. The tubular cell proliferation and apoptosis occurred in the early phase after induction of acute tubular necrosis and the excess hyperplastic epithelial cells appeared to be eliminated by apoptosis. Acute tubular necrosis (ATN) is the most common cause of acute renal failure, and characterized by destruction of tubular epithelial cells. METHODS: To elucidate the role of tubular expression of FasL in the course of acute tubular necrosis, we induced acute renal failure by intramuscular glycerol injection to New Zealand White rabbits and studied the sequential expression of FasL by immunohistochemistry. RESULTS: Acute tubular injury with pigment casts and interstitial hemorrhage were diffusely noted. There was no expression of FasL in normal kidney tissue. Tubular expression of FasL was increased after 4 hours and peaked at 3 days and then gradually decreased at 7 days. CONCLUSION: FasL was expressed by renal tubular cells and its expression increased during acute renal injury. Activation of the FasL may promote tubular apoptosis. These data suggested that FasL may play a pathogenetic role in acute tubular necrosis through apoptotic cascades. These facts imply that the FasL/Fas system can be considered a new target for therapeutic intervention in kidney damage.
