Linked Life Data

2686605

Source:http://linkedlifedata.com/resource/pubmed/id/2686605

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1990-1-2
pubmed:abstractText
Treatment of rabbit aortic endothelial cells or human umbilical vein cells for as little as 1 day with 25 micrograms/ml of beta-migrating very low density lipoprotein (beta-VLDL), but not low density lipoprotein (LDL), caused an increased binding of human peripheral blood monocytes to the endothelium. This increase was maximal by 24 hours but was not significant at 4 hours of pre-incubation with beta-VLDL. Neutrophil binding was not significantly stimulated by beta-VLDL treatment of endothelial cells, while endotoxin (LPS) treatment of endothelial cells stimulated both neutrophil and monocyte binding. Antibody to leukocyte function-associated-antigen-1 and to Mo2 inhibited binding to both beta-VLDL-stimulated and LPS-stimulated cells by 25%. The fact that both rabbit and human cells were stimulated by beta-VLDL to bind human monocytes suggests that some mechanisms regulating binding are conserved between species. These studies suggest that beta-VLDL acts like a chronic inflammatory mediator to cause a sustained increase in binding of monocytes to the endothelium.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0276-5047
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
824-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:articleTitle
Beta-very low density lipoprotein pretreatment of endothelial monolayers increases monocyte adhesion.
pubmed:affiliation
Department of Medicine, University of California Los Angeles School of Medicine 90024.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't