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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
1999-1-5
|
| pubmed:abstractText |
Excessive release of nitric oxide (NO) is most likely a crucial pathophysiological pathway leading to pulmonary dysfunction. Thus, repression of supranormal NO production might be one beneficial mechanism of granulocyte-colony stimulating factor (G-CSF) in inflammatory processes. The aim of this study was to investigate the influence of G-CSF on inducible nitric oxide synthase gene expression in the alveolar epithelial cell line L2. We show that G-CSF suppresses interferon-gamma/tumor necrosis factor-alpha (TNF-alpha) induced inducible nitric oxide synthase gene expression detected as inducible nitric oxide synthase cDNA (cDNA concentration was 633 +/- 38 amol/microg total RNA following 24 h incubation with 100 U/ml interferon-gamma/500 U/ml TNF-alpha, and 440 +/- 14 amol/microg total RNA following 24 h incubation with 250 U/ml G-CSF +/- 100 U/ml interferon-gamma/500 U/ml TNF-alpha, respectively). In addition, application of G-CSF resulted in a decreased synthesis of inducible nitric oxide synthase protein and diminished NO release mediated by the cytokines. The suppression of inducible nitric oxide synthase gene expression in L2 cells by G-CSF may represent a beneficial counterregulatory effect on excessive NO synthesis induced by proinflammatory cytokines in the lung.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antiviral Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Granulocyte Colony-Stimulating...,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/RNA,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Oct
|
| pubmed:issn |
0014-2999
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
2
|
| pubmed:volume |
358
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
169-76
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:9808267-Animals,
pubmed-meshheading:9808267-Antiviral Agents,
pubmed-meshheading:9808267-Blotting, Western,
pubmed-meshheading:9808267-Cells, Cultured,
pubmed-meshheading:9808267-Drug Interactions,
pubmed-meshheading:9808267-Enzyme Induction,
pubmed-meshheading:9808267-Epithelium,
pubmed-meshheading:9808267-Female,
pubmed-meshheading:9808267-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:9808267-Granulocyte Colony-Stimulating Factor,
pubmed-meshheading:9808267-Interferon-gamma,
pubmed-meshheading:9808267-Lung,
pubmed-meshheading:9808267-Nitric Oxide Synthase,
pubmed-meshheading:9808267-Polymerase Chain Reaction,
pubmed-meshheading:9808267-RNA,
pubmed-meshheading:9808267-Rats,
pubmed-meshheading:9808267-Rats, Inbred Lew,
pubmed-meshheading:9808267-Tumor Necrosis Factor-alpha
|
| pubmed:year |
1998
|
| pubmed:articleTitle |
Granulocyte-colony stimulating factor inhibits inducible nitric oxide synthase gene expression in pulmonary epithelial cells in vitro.
|
| pubmed:affiliation |
Department of Physiology I, University of Bonn, Germany.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|