Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/13621
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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.date.accessioned2015-05-16T03:30:38Z
dc.date.available2015-05-16T03:30:38Z
dc.date.issued1998-10-01en
dc.identifier.citationKidney International; 54(4): 1052-62en
dc.identifier.govdoc9767521en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/13621en
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.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherCells, Cultureden
dc.subject.otherCollagen.metabolismen
dc.subject.otherDiabetes Mellitus, Experimental.genetics.metabolismen
dc.subject.otherExtracellular Matrix Proteinsen
dc.subject.otherGene Expressionen
dc.subject.otherImmunohistochemistryen
dc.subject.otherIn Situ Hybridizationen
dc.subject.otherKidney.metabolismen
dc.subject.otherMaleen
dc.subject.otherNeoplasm Proteins.geneticsen
dc.subject.otherRNA, Messenger.genetics.metabolismen
dc.subject.otherRatsen
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.identifier.doi10.1046/j.1523-1755.1998.00081.xen
dc.description.pages1052-62en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/9767521en
dc.type.austinJournal Articleen
local.name.researcherJerums, George
item.openairetypeJournal Article-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.author.deptEndocrinology-
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