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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2001-9-4
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pubmed:abstractText |
Hyperglycemia-induced overexpression of prosclerotic transforming growth factor-beta 1 (TGF-beta 1) has been implicated in the pathogenesis of diabetic nephropathy. Since previous in vivo studies demonstrated a renoprotective effect of low-molecular-weight (LMW) heparin in experimental animals, and recent in vitro data showed an interaction of this drug with the overactivated TGF-beta 1 cascade in high glucose- and phorbol ester-stimulated mesangial cells, we studied the molecular mechanism of these effects on TGF-beta 1 gene expression.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0085-2538
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
60
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
935-43
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:11532088-Animals,
pubmed-meshheading:11532088-Binding Sites,
pubmed-meshheading:11532088-Cells, Cultured,
pubmed-meshheading:11532088-Dose-Response Relationship, Drug,
pubmed-meshheading:11532088-Drug Interactions,
pubmed-meshheading:11532088-Gene Expression Regulation,
pubmed-meshheading:11532088-Glomerular Mesangium,
pubmed-meshheading:11532088-Glucose,
pubmed-meshheading:11532088-Heparin, Low-Molecular-Weight,
pubmed-meshheading:11532088-Phorbol Esters,
pubmed-meshheading:11532088-Promoter Regions, Genetic,
pubmed-meshheading:11532088-Protein Binding,
pubmed-meshheading:11532088-Swine,
pubmed-meshheading:11532088-Transcription Factor AP-1,
pubmed-meshheading:11532088-Transcriptional Activation,
pubmed-meshheading:11532088-Transfection,
pubmed-meshheading:11532088-Transforming Growth Factor beta,
pubmed-meshheading:11532088-Transforming Growth Factor beta1
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pubmed:year |
2001
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pubmed:articleTitle |
Low-molecular-weight heparin prevents high glucose- and phorbol ester-induced TGF-beta 1 gene activation.
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pubmed:affiliation |
Department of Internal Medicine, Division of Endocrinology, Metabolism and Pathobio-chemistry, University of Tübingen, Tübingen, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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