Source:http://linkedlifedata.com/resource/pubmed/id/12907144
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2003-8-8
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pubmed:abstractText |
Abnormalities in smooth muscle cell (SMC) proliferation and differentiation underlie the pathogenesis of proliferative vascular diseases. MDA-7 (HUGO approved symbol IL24) is a unique gene, originally identified as a tumor suppressor and more recently shown to have cytokine activity. MDA-7/IL24 has been implicated in apoptosis and cellular differentiation in tumor cells and in tumor invasion/metastasis in clinical specimens-properties central to SMC remodeling during proliferative vascular diseases. In this study, we evaluated the effects of overexpressing MDA-7/IL24 in various SMC: the apparently "normal" rat PAC1 cell line, primary human coronary artery SMC, and normal rat aortic SMC. We transduced SMC with adenovirus-mda7 (Ad-mda7) or control virus (Ad-Luc) and assessed cell viability, apoptosis, and migration. Ad-mda7 suppressed PAC1 cell growth in a dose-dependent manner while having no effect on normal primary human coronary artery cells or rat aortic SMC, despite strong expression of the MDA-7 transgene in all SMC. Similarly, Ad-mda7 treatment induced apoptosis in PAC1 cells with essentially no effect on normal coronary and rat aortic SMC. Ad-mda7 also inhibited serum-stimulated PAC1 cell migration. Karyotype analysis of PAC1 cells revealed that they exhibit multiple chromosomal aberrations. Importantly, recombinant MDA-7 did not elicit cell death or STAT-3 activation in PAC1 SMC, suggesting that the effects of Ad-mda7 were mediated through an intracellular pathway. These data demonstrate that Ad-mda7 exhibits selectivity in apoptosis induction and growth suppression in an atypical SMC line, raising new questions pertaining to heterogeneity in SMC death susceptibility.
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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 |
Aug
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pubmed:issn |
1525-0016
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
220-9
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12907144-Adenoviridae,
pubmed-meshheading:12907144-Animals,
pubmed-meshheading:12907144-Apoptosis,
pubmed-meshheading:12907144-Cell Division,
pubmed-meshheading:12907144-Cell Movement,
pubmed-meshheading:12907144-Cells, Cultured,
pubmed-meshheading:12907144-Gene Expression,
pubmed-meshheading:12907144-Genes, Tumor Suppressor,
pubmed-meshheading:12907144-Humans,
pubmed-meshheading:12907144-Interleukins,
pubmed-meshheading:12907144-Myocytes, Smooth Muscle,
pubmed-meshheading:12907144-Rats,
pubmed-meshheading:12907144-Transduction, Genetic
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pubmed:year |
2003
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pubmed:articleTitle |
Tumor suppressor MDA-7/IL-24 selectively inhibits vascular smooth muscle cell growth and migration.
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pubmed:affiliation |
Center for Cardiovascular Research, University of Rochester Medical Center, 601 Elmwood Avenue, Box 679, Rochester, New York 14642, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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