Source:http://linkedlifedata.com/resource/pubmed/id/10706724
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2000-3-28
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pubmed:databankReference | |
pubmed:abstractText |
P- and E-selectin are surface glycoproteins that mediate leukocyte rolling on the surface of endothelium in inflammation. We have cloned porcine P-selectin cDNA and generated a mAb, 12C5, with which to examine P-selectin expression by porcine aortic endothelial cells (PAEC) in comparison with that of E-selectin. Basal expression by PAEC of P-selectin was greater than that of E-selectin, whereas E-selectin expression was more prominently enhanced than that of P-selectin by stimulation with TNF-alpha or IL-1alpha. Both human or porcine IL-4 led to an increase in P-selectin expression, with kinetics that were delayed compared with those seen following stimulation with TNF-alpha or IL-1alpha, but IL-4 did not stimulate expression of E-selectin. When cells were stimulated with TNF-alpha in the presence of IL-4, we observed enhanced P-selectin expression with a parallel reduction in E-selectin expression. Finally, the increase in P-selectin expression due to human IL-4 was reduced in the presence of porcine but not human IFN-gamma. These observations show that E-selectin and P-selectin expression are differentially regulated in PAEC, and that IL-4 leads to a shift in the relative surface density of the two molecules toward P-selectin. The ability of porcine IFN-gamma to inhibit IL-4-induced P-selectin expression suggests that the balance between Th1 and Th2 cytokine production may determine the relative densities of the two selectins in chronic immune-mediated inflammation. Because the increased expression of P-selectin induced by human IL-4 was not inhibited by human IFN-gamma, this balance may be shifted toward P-selectin expression in porcine xenografts infiltrated by human lymphocytes.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Complementary,
http://linkedlifedata.com/resource/pubmed/chemical/E-Selectin,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Ligands,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/P-Selectin,
http://linkedlifedata.com/resource/pubmed/chemical/P-selectin ligand protein,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
164
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3309-15
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:10706724-Amino Acid Sequence,
pubmed-meshheading:10706724-Animals,
pubmed-meshheading:10706724-Antibodies, Monoclonal,
pubmed-meshheading:10706724-Aorta,
pubmed-meshheading:10706724-Cell Adhesion,
pubmed-meshheading:10706724-Cells, Cultured,
pubmed-meshheading:10706724-Cloning, Molecular,
pubmed-meshheading:10706724-DNA, Complementary,
pubmed-meshheading:10706724-Down-Regulation,
pubmed-meshheading:10706724-E-Selectin,
pubmed-meshheading:10706724-Endothelium, Vascular,
pubmed-meshheading:10706724-Humans,
pubmed-meshheading:10706724-Interferon-gamma,
pubmed-meshheading:10706724-Interleukin-1,
pubmed-meshheading:10706724-Interleukin-4,
pubmed-meshheading:10706724-Leukocytes,
pubmed-meshheading:10706724-Ligands,
pubmed-meshheading:10706724-Membrane Glycoproteins,
pubmed-meshheading:10706724-Molecular Sequence Data,
pubmed-meshheading:10706724-P-Selectin,
pubmed-meshheading:10706724-Swine,
pubmed-meshheading:10706724-Time Factors,
pubmed-meshheading:10706724-Tumor Necrosis Factor-alpha
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pubmed:year |
2000
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pubmed:articleTitle |
TNF-alpha, IL-4, and IFN-gamma regulate differential expression of P- and E-selectin expression by porcine aortic endothelial cells.
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pubmed:affiliation |
British Heart Foundation Cardiovascular Medicine Unit, and Department of Medicine, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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