Source:http://linkedlifedata.com/resource/pubmed/id/10733549
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2000-4-19
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pubmed:abstractText |
Liver myofibroblasts are major actors in the development of liver fibrosis and cancer progression. There is a large interest in drugs that might deactivate these cells. Many studies have shown that the grapevine-derived polyphenol, trans-resveratrol, and other stilbenes have therapeutic potential in some diseases. In this work, we have studied the effect of grapevine polyphenols on cultured human liver myofibroblasts. We have shown that trans-resveratrol profoundly affects myofibroblast phenotype. Trans-resveratrol induced morphological modifications. It markedly reduced proliferation of myofibroblasts in a dose-dependent manner. Trans-resveratrol also decreased the expression of alpha smooth muscle actin (alpha-SMA) without affecting vimentin or beta-cytoplasmic actin expression. It decreased myofibroblast migration in a monolayer wounding assay. We also showed that trans-resveratrol inhibited the messenger RNA (mRNA) expression of type I collagen. Finally, it decreased the secretion of matrix metalloproteinase 2 (MMP-2). We conclude that trans-resveratrol can deactivate human liver myofibroblasts. In the second part of this study, we have shown that neither trans-piceid (a glycosylated analog) nor trans-piceatannol (a hydroxylated analog) reproduces trans-resveratrol effects on liver myofibroblasts. We finally show that, although trans-resveratrol decreases the proliferation of skin fibroblast and vascular smooth muscle cells, it does not affect their expression of alpha-SMA, which indicates some cell specificity.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Actins,
http://linkedlifedata.com/resource/pubmed/chemical/Antioxidants,
http://linkedlifedata.com/resource/pubmed/chemical/Matrix Metalloproteinase 2,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Procollagen,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Stilbenes,
http://linkedlifedata.com/resource/pubmed/chemical/resveratrol
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0270-9139
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
31
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
922-31
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:10733549-Actins,
pubmed-meshheading:10733549-Antioxidants,
pubmed-meshheading:10733549-Cell Division,
pubmed-meshheading:10733549-Cell Movement,
pubmed-meshheading:10733549-Cells, Cultured,
pubmed-meshheading:10733549-Enzyme Activation,
pubmed-meshheading:10733549-Fibroblasts,
pubmed-meshheading:10733549-Gene Expression,
pubmed-meshheading:10733549-Humans,
pubmed-meshheading:10733549-Liver,
pubmed-meshheading:10733549-Matrix Metalloproteinase 2,
pubmed-meshheading:10733549-Microscopy, Electron,
pubmed-meshheading:10733549-Mitogen-Activated Protein Kinase 1,
pubmed-meshheading:10733549-Mitogen-Activated Protein Kinase 3,
pubmed-meshheading:10733549-Mitogen-Activated Protein Kinases,
pubmed-meshheading:10733549-Muscle, Smooth, Vascular,
pubmed-meshheading:10733549-Procollagen,
pubmed-meshheading:10733549-RNA, Messenger,
pubmed-meshheading:10733549-Stem Cells,
pubmed-meshheading:10733549-Stilbenes
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pubmed:year |
2000
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pubmed:articleTitle |
Deactivation of cultured human liver myofibroblasts by trans-resveratrol, a grapevine-derived polyphenol.
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pubmed:affiliation |
Groupe de Recherches pour l'Etude du Foie INSERM E9917, Faculté des Sciences Pharmaceutiques, Université Victor Segalen Bordeaux 2, Bordeaux, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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