pubmed-article:12684813 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12684813 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:12684813 | lifeskim:mentions | umls-concept:C0235989 | lld:lifeskim |
pubmed-article:12684813 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
pubmed-article:12684813 | lifeskim:mentions | umls-concept:C0475264 | lld:lifeskim |
pubmed-article:12684813 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:12684813 | pubmed:dateCreated | 2003-5-7 | lld:pubmed |
pubmed-article:12684813 | pubmed:abstractText | Transforming growth factor beta 1 (TGF-beta 1) contributes to the accumulation of extracellular matrix (ECM) in the tubulointerstitial space in chronic renal diseases. Identification of target cells and the contribution of epithelial-mesenchymal transformation (EMT) in TGF-beta 1-induced fibrosis in vivo are currently under investigation. We have developed a transgenic model of slowly developing TGF-beta 1-driven tubulointerstitial fibrosis (TIF). By using this model our aim was to localise the ECM-producing cells, to investigate the temporal and spatial distribution of the cellular markers alpha-smooth muscle cell actin (alpha SM-actin), Fsp1 and Hsp47 and to explore the possible involvement of EMT in TGF-beta1-induced TIF in vivo. We utilised a combination of in situ hybridisation, immunohistochemistry and western blotting techniques and found that alpha SM-actin-positive interstitial cells are the main source of collagen types I and III and fibronectin, whereas collagen type IV(alpha 1/alpha 2) originates mainly from the tubular epithelial cells. Furthermore, macrophages are not important combatants during the early course of TGF-beta 1-induced TIF. Finally, EMT is not necessary for the initiation of TGF-beta 1-induced TIF. We conclude, that intervention directed against the recruitment of activated interstitial cells may avoid the development of end-stage renal disease. | lld:pubmed |
pubmed-article:12684813 | pubmed:language | eng | lld:pubmed |
pubmed-article:12684813 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12684813 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:12684813 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12684813 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:12684813 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12684813 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12684813 | pubmed:month | Apr | lld:pubmed |
pubmed-article:12684813 | pubmed:issn | 0948-6143 | lld:pubmed |
pubmed-article:12684813 | pubmed:author | pubmed-author:LedetThomasT | lld:pubmed |
pubmed-article:12684813 | pubmed:author | pubmed-author:WogensenLiseL | lld:pubmed |
pubmed-article:12684813 | pubmed:author | pubmed-author:ChaiQingQ | lld:pubmed |
pubmed-article:12684813 | pubmed:author | pubmed-author:KragSørenS | lld:pubmed |
pubmed-article:12684813 | pubmed:author | pubmed-author:ChaiSongS | lld:pubmed |
pubmed-article:12684813 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12684813 | pubmed:volume | 119 | lld:pubmed |
pubmed-article:12684813 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12684813 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12684813 | pubmed:pagination | 267-80 | lld:pubmed |
pubmed-article:12684813 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:12684813 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12684813 | pubmed:articleTitle | Localisation and phenotypical characterisation of collagen-producing cells in TGF-beta 1-induced renal interstitial fibrosis. | lld:pubmed |
pubmed-article:12684813 | pubmed:affiliation | The Research Laboratory for Biochemical Pathology, The Institute for Experimental Clinical Research, Aarhus Kommunehospital, 44-Noerrebrogade, 8000 Aarhus C, Denmark. | lld:pubmed |
pubmed-article:12684813 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12684813 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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