| Identification of TGF-β-induced Gene Product, βig-h3 in Ischemic Acute Renal Failure |
| Min-Jeong Choi, M.D.1, Sun-Hee Park, M.D.1, Chan-Duck Kim, M.D.1, Yong-Lim Kim, M.D.1 Tae-Hwan Kwon, M.D.2, In-San Kim, M.D.2 and Yong-Jin Kim, M.D.3 |
Department of Internal Medicine1
Kyungpook National University Hospital Department of Biochemistry and Cell and Matrix Research Institute Kyungpook National University School of Medicine2 Department of Pathology, Yeungnam University College of Medicine3
Daegu, Korea |
| 허혈성 급성신부전에서 TGF-β-induced gene product βig-h3의 변화와 초기 표지자로서의 의의 |
| 최민정1 박선희1 김찬덕1 김용림1 권태환2 김인산2 김용진3 |
| 경북대학교 의과대학 내과학교실1, 경북대학교 의과대학 생화학 세포생물학 교실2, 영남대학교 의과대학 병리학교실3 |
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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. |
| Key Words:
Acute renal failure, Reperfusion injury, TGF-beta, betaIG-H3 protein |
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