Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1997-7-10
pubmed:abstractText
There is evidence to suggest that elevated plasma levels of lipoprotein (a) [Lp(a)] represent a risk factor for the development of atherosclerotic vascular disease, but the mechanism by which this lipoprotein localizes to involved vessels is only partially understood. In view of studies suggesting a link between inflammation and atherosclerosis and our previous finding that leukocyte defensin modulates the interaction of plasminogen and tissue-type plasminogen activator with cultured human endothelial cells, we examined the effect of this peptide on the binding of Lp(a) to cultured vascular endothelium and vascular smooth muscle cells. Defensin increased the binding of Lp(a) to endothelial cells approximately fourfold and to smooth muscle cells approximately sixfold. Defensin caused a comparable increase in the amount of Lp(a) internalized by each cell type, but Lp(a) internalized as a consequence of defensin being present was not degraded, resulting in a marked increase in the total amount of cell-associated lipoprotein. Abundant defensin was found in endothelium and in intimal smooth muscle cells of atherosclerotic human cerebral arteries, regions also invested with Lp(a). These studies suggest that defensin released from activated or senescent neutrophils may contribute to the localization and persistence of Lp(a) in human vessels and thereby predispose to the development of atherosclerosis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
89
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4290-8
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:9192751-Adult, pubmed-meshheading:9192751-Aged, pubmed-meshheading:9192751-Aged, 80 and over, pubmed-meshheading:9192751-Aortic Diseases, pubmed-meshheading:9192751-Apolipoproteins, pubmed-meshheading:9192751-Apoprotein(a), pubmed-meshheading:9192751-Arteriosclerosis, pubmed-meshheading:9192751-Blood Proteins, pubmed-meshheading:9192751-Cells, Cultured, pubmed-meshheading:9192751-Cerebral Arteries, pubmed-meshheading:9192751-Coronary Artery Disease, pubmed-meshheading:9192751-Defensins, pubmed-meshheading:9192751-Endocytosis, pubmed-meshheading:9192751-Endothelium, Vascular, pubmed-meshheading:9192751-Female, pubmed-meshheading:9192751-Humans, pubmed-meshheading:9192751-Leukocytes, pubmed-meshheading:9192751-Lipoprotein(a), pubmed-meshheading:9192751-Macromolecular Substances, pubmed-meshheading:9192751-Male, pubmed-meshheading:9192751-Middle Aged, pubmed-meshheading:9192751-Muscle, Smooth, Vascular, pubmed-meshheading:9192751-Protein Binding, pubmed-meshheading:9192751-Stimulation, Chemical, pubmed-meshheading:9192751-Umbilical Veins, pubmed-meshheading:9192751-Vasculitis
pubmed:year
1997
pubmed:articleTitle
Defensin stimulates the binding of lipoprotein (a) to human vascular endothelial and smooth muscle cells.
pubmed:affiliation
Department of Pathology, University of Pennsylvania Medical Center, Philadelphia, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't