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KMID : 0359920070260030301
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Korean Journal of Nephrology
2007 Volume.26 No. 3 p.301 ~ p.310
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Identification of TGF-β-induced Gene Product, βig-h3 in Ischemic Acute Renal Failure
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Choi Min-Jeong
Park Sun-Hee
Kim Chan-Duck
Kim Yong-Lim
KwonTae-Hwan
Kim In-San
Kim Yong-Jin
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Abstract
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Purpose : Acute renal failure remains a potentially devastating clinical problem. This study aimed to
examine whether the expression of TGF-β-induced gene product, βig-h3, is altered in ischemiareperfusion
(I/R) injury and urinary excretion of βig-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-β and βig-h3 were measured after I/R injury. Also, the renal expression of βig-h3
by western blotting and immunohistochemistry were investigated. In the second step, urinary βig-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 βig-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 βig-h3 expression.
Immunohistochemistry showed that labeling of βig-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 βig-h3 was significantly increased at 4 hours after I/R injury.
Importantly, the urinary appearance of βig-h3 preceded that of N-acetyl-β-D-glucosaminidase.
Conclusion : These results suggest that endogenous renal βig-h3 may serve to promote tissue
regeneration in I/R injury and urinary βig-h3 could be used as an early and sensitive marker demonstrating
I/R injury.
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KEYWORD
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Acute renal failure, Reperfusion injury, TGF-beta, betaIG-H3 protein
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