| pubmed-article:17200187 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17200187 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
| pubmed-article:17200187 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
| pubmed-article:17200187 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:17200187 | lifeskim:mentions | umls-concept:C0151650 | lld:lifeskim |
| pubmed-article:17200187 | lifeskim:mentions | umls-concept:C0123744 | lld:lifeskim |
| pubmed-article:17200187 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:17200187 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:17200187 | pubmed:dateCreated | 2007-1-3 | lld:pubmed |
| pubmed-article:17200187 | pubmed:abstractText | The transforming growth factor (TGF)-beta-inducible integrin alpha v beta6 is preferentially expressed at sites of epithelial remodeling and has been shown to bind and activate latent precursor TGF-beta. Herein, we show that alpha v beta6 is overexpressed in human kidney epithelium in membranous glomerulonephritis, diabetes mellitus, IgA nephropathy, Goodpasture's syndrome, and Alport syndrome renal epithelium. To assess the potential regulatory role of alpha v beta6 in renal disease, we studied the effects of function-blocking alpha v beta6 monoclonal antibodies (mAbs) and genetic ablation of the beta6 subunit on kidney fibrosis in Col4A3-/- mice, a mouse model of Alport syndrome. Expression of alpha v beta6 in Alport mouse kidneys was observed primarily in cortical tubular epithelial cells and in correlation with the progression of fibrosis. Treatment with alpha v beta6-blocking mAbs inhibited accumulation of activated fibroblasts and deposition of interstitial collagen matrix. Similar inhibition of renal fibrosis was observed in beta6-deficient Alport mice. Transcript profiling of kidney tissues showed that alpha v beta6-blocking mAbs significantly inhibited disease-associated changes in expression of fibrotic and inflammatory mediators. Similar patterns of transcript modulation were produced with recombinant soluble TGF-beta RII treatment, suggesting shared regulatory functions of alpha v beta6 and TGF-beta. These findings demonstrate that alpha v beta6 can contribute to the regulation of renal fibrosis and suggest this integrin as a potential therapeutic target. | lld:pubmed |
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| pubmed-article:17200187 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17200187 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17200187 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:17200187 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17200187 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:17200187 | pubmed:issn | 0002-9440 | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:ItoRR | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:SheppardDeanD | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:KalluriRaghuR | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:GardnerHumphr... | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:LobbRoy RRR | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:McCrannDonald... | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:FogoAgnesA | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:ShieldCharles... | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:WeinrebPaul... | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:YangWilliam... | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:VioletteSheli... | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:SimonKenneth... | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:LukashevMatve... | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:LeoneDiane... | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:DolinskiBrian... | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:HahmKyungminK | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:AllaireNorman... | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:Chun WangLiL | lld:pubmed |
| pubmed-article:17200187 | pubmed:author | pubmed-author:HoranGerald... | lld:pubmed |
| pubmed-article:17200187 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17200187 | pubmed:volume | 170 | lld:pubmed |
| pubmed-article:17200187 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17200187 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17200187 | pubmed:pagination | 110-25 | lld:pubmed |
| pubmed-article:17200187 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:17200187 | pubmed:meshHeading | pubmed-meshheading:17200187... | lld:pubmed |
| pubmed-article:17200187 | pubmed:meshHeading | pubmed-meshheading:17200187... | lld:pubmed |
| pubmed-article:17200187 | pubmed:meshHeading | pubmed-meshheading:17200187... | lld:pubmed |
