Source:http://linkedlifedata.com/resource/pubmed/id/17949278
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
11
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| pubmed:dateCreated |
2007-10-22
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| pubmed:abstractText |
Monocyte chemoattractant protein-1 (MCP-1) is produced by different cells in response to inflammatory stimulation. In the present study, a series of human MCP-1 promoter reporter genes were constructed to illustrate elements involved in antioxidant dimethyl sulfoxide (DMSO) inhibition of MCP-1 gene expression. MCP-1 secretion and mRNA expression and transcription activity stimulated by TNF-alpha or IL-1beta were significantly inhibited by 1% DMSO in alveolar type II epithelial cells (A549). Deletion of -7537 to -2741 caused a 77% decrease in reporter activity, but DMSO inhibition was still present. Deletion of -7537 to -2616 containing the A1 NF-kappaB binding site resulted in a complete loss of MCP-1 stimulation. Deletion of -2585 to -74 decreased reporter activity by approximately 50%, and DMSO inhibited this induction. Deletion of -2614 to -74 containing the A2 NF-kappaB binding site completely abolished responses to stimulation. Mutations of either of the NF-kappaB binding sites decreased promoter activity, which could still be inhibited by DMSO, whereas deletion of both NF-kappaB binding sites abolished induced transcriptional activity. Mutation or deletion of the NF-kappaB binding sites significantly decreased or abolished reporter activity in response to reactive oxygen intermediates (ROI), generated by xanthine plus xanthine oxidase. In conclusion, DMSO inhibits MCP-1 gene expression through both NF-kappaB binding sites located far upstream of the 5'-flanking region of the MCP-1 promoter.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antioxidants,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL2,
http://linkedlifedata.com/resource/pubmed/chemical/Dimethyl Sulfoxide,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1beta,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Luciferases,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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| pubmed:status |
MEDLINE
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| pubmed:month |
Nov
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| pubmed:issn |
1523-0864
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
9
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1979-89
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| pubmed:dateRevised |
2010-12-3
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| pubmed:meshHeading |
pubmed-meshheading:17949278-Antioxidants,
pubmed-meshheading:17949278-Cell Line,
pubmed-meshheading:17949278-Chemokine CCL2,
pubmed-meshheading:17949278-Dimethyl Sulfoxide,
pubmed-meshheading:17949278-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:17949278-Epithelial Cells,
pubmed-meshheading:17949278-Gene Expression Regulation,
pubmed-meshheading:17949278-Genes, Reporter,
pubmed-meshheading:17949278-Humans,
pubmed-meshheading:17949278-Interleukin-1beta,
pubmed-meshheading:17949278-Interleukin-6,
pubmed-meshheading:17949278-Lipopolysaccharides,
pubmed-meshheading:17949278-Luciferases,
pubmed-meshheading:17949278-Lung,
pubmed-meshheading:17949278-Promoter Regions, Genetic,
pubmed-meshheading:17949278-RNA, Messenger,
pubmed-meshheading:17949278-Time Factors,
pubmed-meshheading:17949278-Transfection,
pubmed-meshheading:17949278-Tumor Necrosis Factor-alpha
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| pubmed:year |
2007
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| pubmed:articleTitle |
Promoter elements responsible for antioxidant regulation of MCP-1 gene expression.
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| pubmed:affiliation |
Department of Pathology University of Michigan, Medical School, Ann Arbor, Michigan 48109, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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