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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1997-1-9
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pubmed:abstractText |
Diabetic nephropathy is associated with thickening of the glomerular basement membrane and, in particular, with mesangial matrix expansion. Previous studies have indicated that administration of chemically modified, low-anticoagulant heparins prevents some of the morphologic and physiologic alterations occurring in experimental diabetic nephropathy. The effect of prolonged heparin treatment on the glomerular expression and deposition of alpha 1 (IV) collagen, which is a major component of the mesangial matrix, has not been reported previously. Four groups of rats were studied for 12 months: two control groups and two groups of streptozotocin-diabetic rats. One group in each branch received modified heparin continuously from the induction of diabetes. After 12 months synthesis and deposition of alpha 1 (IV) collagglomerula and adjacent tubuli were determined by nonradioactive in situ hybridization and immunohistochemistry. Mesangial cells were localized by Thy 1.1 staining. Long-term diabetes caused a significant increase in alpha 1 (IV) collagen deposition in the mesangial matrix and a more than 2-fold enhancement of glomerular cell alpha 1 (IV) collagen transcript levels, mainly in mesangial cells. The alpha 1 (IV) collagen mRNA levels of proximal tubular cells and visceral epithelial cells were similarly increased. Chronic treatment of diabetic rats with modified heparin completely prevented the increased alpha 1 (IV) collagen deposition and expression. The increased glomerular deposition of alpha 1 (IV) collagen observed in long-term streptozotocin diabetic rats appears to depend on an increased alpha 1 (IV) collagen synthesis. Because chronic application of low-anticoagulant heparin completely prevents the increased alpha 1 (IV) collagen synthesis by mesangial cells, this result suggests a new therapeutic option for the prevention of diabetic nephropathy in humans.
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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 |
Feb
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pubmed:issn |
0023-6837
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
74
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
484-95
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8780166-Animals,
pubmed-meshheading:8780166-Chronic Disease,
pubmed-meshheading:8780166-Collagen,
pubmed-meshheading:8780166-Diabetes Mellitus, Experimental,
pubmed-meshheading:8780166-Drug Administration Schedule,
pubmed-meshheading:8780166-Glycosaminoglycans,
pubmed-meshheading:8780166-Heparin,
pubmed-meshheading:8780166-In Situ Hybridization,
pubmed-meshheading:8780166-Kidney Glomerulus,
pubmed-meshheading:8780166-Male,
pubmed-meshheading:8780166-RNA, Messenger,
pubmed-meshheading:8780166-Rats,
pubmed-meshheading:8780166-Rats, Sprague-Dawley
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pubmed:year |
1996
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pubmed:articleTitle |
Increased glomerular alpha 1 (IV) collagen expression and deposition in long-term diabetic rats is prevented by chronic glycosaminoglycan treatment.
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pubmed:affiliation |
Department of Nephrology, University of Padua, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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