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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0022646,
umls-concept:C0035015,
umls-concept:C0040690,
umls-concept:C0086418,
umls-concept:C0205178,
umls-concept:C0205191,
umls-concept:C0331858,
umls-concept:C0450127,
umls-concept:C0522536,
umls-concept:C1171362,
umls-concept:C1548437,
umls-concept:C1704640,
umls-concept:C1706515,
umls-concept:C1882923
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pubmed:issue |
2
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pubmed:dateCreated |
1995-12-22
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pubmed:abstractText |
Because the increased tissue expression of TGF-beta underlies fibrosis in many diseases, it was hypothesized that sustained elevated transforming growth factor (TGF)-beta overexpression might be responsible for fibrosis in chronic rejection of the renal allograft. To test this hypothesis, biopsies were obtained from 5 patients with acute rejection, 5 patients with chronic rejection, 10 normal individuals, and 10 patients with kidney disease. The tissues were examined by immunofluorescence for the three TGF-beta isoforms (1, 2, and 3) and the two matrix proteins induced by TGF-beta that serve as markers of fibrosis: fibronectin extradomain A positive (EDA+) and plasminogen activator inhibitor-1 (PAI-1). The tubulointerstitium from all cases of acute rejection and chronic rejection showed highly significant increases in immunostaining for the three TGF-beta isoforms (P < 0.001), fibronectin EDA+ (P < 0.005), and PAI-1 (P < 0.001). In the glomeruli, only TGF-beta 1 expression achieved statistical significance (P < 0.005) in acute rejection, whereas in chronic rejection, all three TGF-beta isoforms (p < 0.001) in addition to fibronectin EDA+ (p < 0.001) and PAI-1 (p < 0.001) were elevated. There was both cellular and matrix staining of the TGF-beta isoforms. In striking contrast, control kidney tissues were negative or only weakly positive. Because TGF-beta was present both in acute and in chronic rejection but not in control tissues and because acute rejection episodes are a good predictor for chronic rejection, these results suggest that TGF-beta may play a role in the pathogenesis of fibrosis in chronic rejection.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1046-6673
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
6
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
286-94
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:7579098-Acute Disease,
pubmed-meshheading:7579098-Chronic Disease,
pubmed-meshheading:7579098-Fibronectins,
pubmed-meshheading:7579098-Graft Rejection,
pubmed-meshheading:7579098-Humans,
pubmed-meshheading:7579098-Kidney Transplantation,
pubmed-meshheading:7579098-Plasminogen Activator Inhibitor 1,
pubmed-meshheading:7579098-Transforming Growth Factor beta
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pubmed:year |
1995
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pubmed:articleTitle |
Transforming growth factor-beta and matrix protein expression in acute and chronic rejection of human renal allografts.
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pubmed:affiliation |
Division of Nephrology, University of Utah School of Medicine, Salt Lake City 84132, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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