Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/13621
Title: Renal expression of transforming growth factor-beta inducible gene-h3 (beta ig-h3) in normal and diabetic rats.
Authors: Gilbert, Richard E;Wilkinson-Berka, J L;Johnson, D W;Cox, Allison J;Soulis, T;Wu, L L;Kelly, D J;Jerums, George;Pollock, C A;Cooper, Mark E
Affiliation: University of Melbourne Department of Medicine, Victoria, Australia. gilbert@austin.unimelb.edu.au
Issue Date: 1-Oct-1998
Citation: Kidney International; 54(4): 1052-62
Abstract: Transforming growth factor-beta (TGF-beta) has been implicated in the pathogenesis of a number of kidney diseases characterized by glomerulosclerosis and tubulointerstitial fibrosis. TGF-beta is secreted in a latent form requiring extracellular modification to become biologically active. TGF-beta inducible gene-h3 (beta ig-h3) is a recently identified TGF-beta-induced gene product. The present study sought to examine beta ig-h3 expression in normal and diabetic rats.Beta ig-h3, TGF-beta1 and alpha1 (IV) collagen gene expression were assessed by Northern blot analysis and in situ hybridization in 20 Sprague Dawley rats, randomly assigned to receive streptozotocin (diabetic, N = 11) or citrate buffer alone (control, N = 9) and sacrificed eight months later. The effect of exogenous TGF-beta1 on beta ig-h3 expression was also assessed in cultured proximal tubular cells.In situ hybridization localized beta ig-h3 gene expression to the juxtaglomerular apparatus and the pars recta (S3 segment) of proximal tubules in both control and diabetic animals. Kidney TGF-beta 1, beta ig-h3 and alpha1 (IV) collagen mRNA from diabetic rats were increased two- to threefold compared with controls (P < 0.01). There was a significant correlation between TGF-beta1 and beta ig-h3 gene expression in kidneys from diabetic rats (r = 0.73, P = 0.01). In addition, beta ig-h3 mRNA increased in response to exogenous TGF-beta1 in a dose-dependent fashion in cultured proximal tubular cells.These findings support the hypothesis that biologically active TGF-beta plays a pathogenetic role in diabetic kidney disease and suggest that beta ig-h3 may be a useful index of TGF-beta1 bioactivity in the kidney.
Internal ID Number: 9767521
URI: http://ahro.austin.org.au/austinjspui/handle/1/13621
DOI: 10.1046/j.1523-1755.1998.00081.x
URL: http://www.ncbi.nlm.nih.gov/pubmed/9767521
Type: Journal Article
Subjects: Animals
Cells, Cultured
Collagen.metabolism
Diabetes Mellitus, Experimental.genetics.metabolism
Extracellular Matrix Proteins
Gene Expression
Immunohistochemistry
In Situ Hybridization
Kidney.metabolism
Male
Neoplasm Proteins.genetics
RNA, Messenger.genetics.metabolism
Rats
Rats, Sprague-Dawley
Transforming Growth Factor beta.genetics
Appears in Collections:Journal articles

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