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dc.contributor.authorGilbert, Richard Een
dc.contributor.authorWilkinson-Berka, J Len
dc.contributor.authorJohnson, D Wen
dc.contributor.authorCox, Allison Jen
dc.contributor.authorSoulis, Ten
dc.contributor.authorWu, L Len
dc.contributor.authorKelly, D Jen
dc.contributor.authorJerums, Georgeen
dc.contributor.authorPollock, C Aen
dc.contributor.authorCooper, Mark Een
dc.identifier.citationKidney International; 54(4): 1052-62en
dc.description.abstractTransforming 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.en
dc.subject.otherCells, Cultureden
dc.subject.otherDiabetes Mellitus, Experimental.genetics.metabolismen
dc.subject.otherExtracellular Matrix Proteinsen
dc.subject.otherGene Expressionen
dc.subject.otherIn Situ Hybridizationen
dc.subject.otherNeoplasm Proteins.geneticsen
dc.subject.otherRNA, Messenger.genetics.metabolismen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherTransforming Growth Factor beta.geneticsen
dc.titleRenal expression of transforming growth factor-beta inducible gene-h3 (beta ig-h3) in normal and diabetic rats.en
dc.typeJournal Articleen
dc.identifier.journaltitleKidney Internationalen
dc.identifier.affiliationUniversity of Melbourne Department of Medicine, Victoria, Australiaen
dc.type.austinJournal Articleen, George
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
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