Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2000-3-28
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
164
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3309-15
pubmed:dateRevised
2008-11-21
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
pubmed:year
2000
pubmed:articleTitle
TNF-alpha, IL-4, and IFN-gamma regulate differential expression of P- and E-selectin expression by porcine aortic endothelial cells.
pubmed:affiliation
British Heart Foundation Cardiovascular Medicine Unit, and Department of Medicine, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't