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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1986-2-5
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pubmed:abstractText |
Cultured human vascular endothelial cells obtained from umbilical cord veins were observed to acquire adhesive properties for purified neutrophils after exposure to IL 1, endotoxin, and tumor-promoting phorbol diesters. Adhesiveness induced by IL1 and endotoxin had similar kinetics of onset, producing no change after 30 min incubation and reaching optimal change by 4 hr of incubation. The phorbol diester TPA induced changes in adhesiveness more rapidly, with half maximal increase induced by a 15- to 30-min exposure. TPA, but not IL 1 or LPS, induced significant morphologic changes in the endothelial cell monolayer. None of the stimuli decreased endothelial cell viability. All stimuli induced increased adhesiveness at relevant concentrations, i.e., endotoxin, 0.01 to 1 microgram/ml; IL 1, 0.5 to 2 U/ml; and TPA, 1 to 30 ng/ml. Structure activity relationships among phorbol diesters indicate that the response occurs through a typical phorbol diester "receptor." A protein synthesis inhibitor (cycloheximide) and an RNA synthesis inhibitor (actinomycin D) prevented the acquisition of adhesiveness stimulated by IL 1 and endotoxin but not by TPA. In addition, TPA showed a differential temperature sensitivity in inducing adhesiveness in endothelial cells. IL 1 and endotoxin did not produce the effect with a 4-hr incubation at 22 degrees or 4 degrees C, whereas TPA was effective at these lower temperatures. Purified human IL 2 and recombinant-derived interferon-gamma failed to induce adhesiveness in vascular endothelial cells, indicating that this is not a general property of lymphokines. We conclude that endothelium may, under some circumstances, play an active role in producing a leukocyte infiltrate at a local tissue site by acquiring adhesive properties. The production of IL 1 by tissue macrophages, etc., may serve as an important initiator of an inflammatory cell infiltrate. Finally, an action of tumor-promoting phorbol diesters in increasing endothelial cell adhesiveness, combined with their known effects in activating leukocytes, may help explain the extraordinary inflammatory potency of these compounds.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Endotoxins,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Phorbols,
http://linkedlifedata.com/resource/pubmed/chemical/RNA,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
136
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
649-54
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:2416819-Cell Adhesion,
pubmed-meshheading:2416819-Cells, Cultured,
pubmed-meshheading:2416819-Dose-Response Relationship, Drug,
pubmed-meshheading:2416819-Endothelium,
pubmed-meshheading:2416819-Endotoxins,
pubmed-meshheading:2416819-Humans,
pubmed-meshheading:2416819-Interferon-gamma,
pubmed-meshheading:2416819-Interleukin-1,
pubmed-meshheading:2416819-Interleukin-2,
pubmed-meshheading:2416819-Kinetics,
pubmed-meshheading:2416819-Neutrophils,
pubmed-meshheading:2416819-Phorbols,
pubmed-meshheading:2416819-Protein Biosynthesis,
pubmed-meshheading:2416819-RNA,
pubmed-meshheading:2416819-Temperature,
pubmed-meshheading:2416819-Tetradecanoylphorbol Acetate,
pubmed-meshheading:2416819-Umbilical Veins
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pubmed:year |
1986
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pubmed:articleTitle |
Cultured human vascular endothelial cells acquire adhesiveness for neutrophils after stimulation with interleukin 1, endotoxin, and tumor-promoting phorbol diesters.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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