Renal Expression and Usefulness of TGF-beta-inducible Gene-h3 in Human Type II Diabetic Nephropathy -Immunohistochemical Analysis-.
- Author:
Soon Won HONG
1
;
Beom Jin LIM
;
Hyeon Joo JEONG
;
Dongsin LEE-YOON
;
Hee Jeong YUN
Author Information
1. Department of Pathology, Yonsei University College of Medicine, Seoul, Korea. soonwonh@yumc.yonsei.ac.kr
- Publication Type:Original Article
- Keywords:
Diabetic nephropathy;
Human;
TGF-beta;
beta ig-h3 protein;
Immunohistochemistry
- MeSH:
Diabetic Nephropathies*;
Epithelium;
Extracellular Matrix;
Humans*;
Hypertrophy;
Immunohistochemistry;
RNA, Messenger;
Transforming Growth Factor beta;
Transforming Growth Factor beta1
- From:Korean Journal of Nephrology
2004;23(4):559-566
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Activation of transforming growth factor-beta (TGF-beta) system has been implicated in the pathological change of diabetic nephropathy such as renal hypertrophy and accumulation of extracellular matrix. In tissues, TGF-beta is secreted as a biologically inactive complex requiring in vivo activation. Thus, increased TGF-beta1 mRNA or protein may not necessarily reflect parallel changes in TGF-beta1 biologic activity. TGF-beta1 inducible gene-h3 (betaig-h3) is a novel gene uniquely up-regulated by active TGF-beta1. METHODS: For evaluating the beta ig-h3 protein expression in human diabetic nephropathy, we examed the expression of beta ig-h3 protein, TGF-beta1, TGF-beta type II receptor (TRII) and Smad protein intranuclear translocation by immunohistochemistry in human diabetic nephropathy tissues (n=11) and normal renal tissue (n=3). RESULTS: The beta ig-h3 protein was expressed in diabetic tubular epithelium (diabetes vs. normal 7/11 vs. 0/3) and diabetic glomerulus (diabetes vs. normal 5/11 vs. 0/3). The tubular expression was stronger than the interstitial expression. The TGF-beta1 was expressed in diabetic tubular epithelium (diabetes vs. normal 1/11 vs. 0/3) and diabetic glomerulus (diabetes vs. normal 3/11 vs. 0/3). The TGF-beta type II was expressed more in diabetic glomerulus (diabetes vs normal 6/11 vs. 1/3). But in the tubule, the expression didn't show any significant difference. The number of intranuclear translocation of Smad protein in glomerulus (diabetes vs normal 49.1+/-0.3 vs. 40.1+/-0.8) was increased in diabetes, but the tubular manifestation was not significant. CONCLUSION: We propose that TGF-beta system mediates human diabetic nephropathy through beta ig- h3 protein expression. The beta ig-h3 protein expression could be a useful marker expecting of disease activity and progress.
