Identification of TGF-beta-induced Gene Product, betaig-h3 in Ischemic Acute Renal Failure.
- Author:
Min Jeong CHOI
1
;
Sun Hee PARK
;
Chan Duck KIM
;
Yong Lim KIM
;
Tae Hwan KWON
;
In San KIM
;
Yong Jin KIM
Author Information
1. Department of Internal Medicine1, Kyungpook National University Hospital, Korea. sh-park@knu.ac.kr
- Publication Type:Original Article
- Keywords:
Acute renal failure;
Reperfusion injury;
TGF-beta;
betaIG-H3 protein
- MeSH:
Acetylglucosaminidase;
Acute Kidney Injury*;
Basement Membrane;
Blotting, Western;
Constriction;
Creatinine;
Epithelial Cells;
Immunohistochemistry;
Regeneration;
Renal Artery;
Reperfusion;
Reperfusion Injury;
Transforming Growth Factor beta
- From:Korean Journal of Nephrology
2007;26(3):301-310
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Acute renal failure remains a potentially devastating clinical problem. This study aimed to examine whether the expression of TGF-beta-induced gene product, betaig-h3, is altered in ischemia- reperfusion (I/R) injury and urinary excretion of betaig-h3 is changed in I/R injury. METHODS: I/R injury was performed by clamping both renal arteries. Daily urine output, serum creatinine and urinary TGF-beta and betaig-h3 were measured after I/R injury. Also, the renal expression of betaig-h3 by western blotting and immunohistochemistry were investigated. In the second step, urinary betaig-h3 was measured at 4, 10, 16, and 24 hours after I/R injury to investigate whether it could be used as an early and sensitive marker for detecting I/R injury. RESULTS: Urinary betaig-h3 was significantly elevated at 24 hours and maintained higher than the controls until 2 days after I/R injury. In contrast, western blotting did not reveal any changes of betaig-h3 expression. Immunohistochemistry showed that labeling of betaig-h3 was seen at the basement membranes of proximal tubule cells mainly located at the medullary ray (S3 segment) in both groups. Following I/R injury, the labeling was also seen in the basement membrane of injured or regenerated proximal tubular epithelial cells. Within 24 hours, urinary betaig-h3 was significantly increased at 4 hours after I/R injury. Importantly, the urinary appearance of betaig-h3 preceded that of N-acetyl-beta-D-glucosaminidase. CONCLUSION: These results suggest that endogenous renal betaig-h3 may serve to promote tissue regeneration in I/R injury and urinary betaig-h3 could be used as an early and sensitive marker demonstrating I/R injury.
