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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1994-10-24
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pubmed:abstractText |
In the present study we investigated the influence of the PKC-inhibitor GF109203X on cytokine- and endotoxin-induced expression of intercellular adhesion molecule 1 (ICAM-1) and on the adhesion of lymphocytes to cytokine-activated endothelial cells. We found that tumour necrosis factor alpha (TNF-alpha)- and lipopolysaccharide (LPS)-induced ICAM-1 expression on a human endothelium-derived cell line (EA.hy926) were unaffected by the PKC-inhibitor and thus appeared to be independent of PKC activation. In contrast, GF109203X significantly reduced ICAM-1 expression induced by interferon-gamma (IFN-gamma) and interleukin-1 (IL-1). The functional relevance of these findings was evaluated in an adhesion assay using human umbilical vein endothelial cells (HUVEC) and peripheral blood mononuclear cells (PBMC). In fact, the IFN-gamma- and IL-1-induced adhesion of PBMC to cytokine treated HUVEC could be down-regulated by the PKC-inhibitor, whereas TNF alpha- and LPS-mediated adhesion was not affected. Additionally, the IL-1-driven ICAM-1 expression on HUVEC as well as the IL-1 induced adhesion of PBMC to HUVEC was found to be TNF-dependent, as both effects could be inhibited by an anti-TNF-alpha monoclonal antibody (MoAb) (MAK195). Based on these data on differential regulation of cytokine-induced lymphocyte-endothelium interactions our study supports the use of PKC-inhibitors as additive modulators in cytokine related pathophysiological conditions.
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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/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Indoles,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Adhesion Molecule-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Maleimides,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/bisindolylmaleimide I
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0300-9475
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
40
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
395-402
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:7939411-Cell Adhesion,
pubmed-meshheading:7939411-Cells, Cultured,
pubmed-meshheading:7939411-Cytokines,
pubmed-meshheading:7939411-Endothelium, Vascular,
pubmed-meshheading:7939411-Flow Cytometry,
pubmed-meshheading:7939411-Humans,
pubmed-meshheading:7939411-Indoles,
pubmed-meshheading:7939411-Intercellular Adhesion Molecule-1,
pubmed-meshheading:7939411-Interferon-gamma,
pubmed-meshheading:7939411-Interleukin-1,
pubmed-meshheading:7939411-Lipopolysaccharides,
pubmed-meshheading:7939411-Lymphocytes,
pubmed-meshheading:7939411-Maleimides,
pubmed-meshheading:7939411-Protein Kinase C,
pubmed-meshheading:7939411-Tumor Necrosis Factor-alpha
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pubmed:year |
1994
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pubmed:articleTitle |
Differential role of protein kinase C in cytokine induced lymphocyte-endothelium interaction in vitro.
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pubmed:affiliation |
GSF-Institut für Klinische Molekularbiologie, München, Germany.
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pubmed:publicationType |
Journal Article
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