Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1992-3-18
pubmed:abstractText
Lipoprotein lipase (LPL), the rate-limiting enzyme for hydrolysis of plasma lipoprotein triglycerides, is a normal constituent of the arterial wall. We explored whether LPL affects (a) lipoprotein transport across bovine aortic endothelial cells or (b) lipoprotein binding to subendothelial cell matrix (retention). When bovine milk LPL was added to endothelial cell monolayers before addition of 125I-labeled LDL, LDL transport across the monolayers was unchanged; but, at all concentrations of LDL tested (1-100 micrograms), LDL retention by the monolayers increased more than fourfold. 125I-labeled LDL binding to extracellular matrix increased when LPL was added directly to the matrix or was added to the basolateral side of the endothelial cell monolayers. Increased LDL binding required the presence of LPL and was not associated with LDL aggregation. LPL also increased VLDL, but not HDL, retention. Monoclonal anti-LPL IgG decreased both VLDL and LDL retention in the presence of LPL. Lipoprotein transport across the monolayers increased during hydrolysis of VLDL triglyceride (TG). In the presence of LPL and VLDL, VLDL transport across the monolayers increased 18% and LDL transport increased 37%. High molar concentrations of oleic acid to bovine serum albumin (3:1) in the medium increased VLDL transport approximately 30%. LDL transport increased 42% when oleic acid was added to the media. Therefore, LPL primarily increased retention of LDL and VLDL. A less remarkable increase in lipoprotein transport was found during hydrolysis of TG-containing lipoproteins. We hypothesize that LPL-mediated VLDL and LDL retention within the arterial wall potentiates conversion of these lipoproteins to more atherogenic forms.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-13252080, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-168000, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-1719546, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-2006165, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-202290, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-2117022, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-2118907, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-222498, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-2226523, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-222756, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-2302416, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-2347922, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-2590068, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-2648148, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-2648155, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-2703536, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-2704743, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-2925647, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-3276735, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-3301850, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-3355847, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-3511384, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-3553402, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-3585176, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-3597382, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-3782469, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-4043407, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-4064263, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-4335139, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-4336380, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-6254083, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-6309127, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-6311077, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-6477300, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-6480690, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-6769124, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-6874679, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-7056857, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-7234961, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-7251587, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-7309739, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-7354064, http://linkedlifedata.com/resource/pubmed/commentcorrection/1737833-7426083
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0021-9738
pubmed:author
pubmed:issnType
Print
pubmed:volume
89
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
373-80
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Lipoprotein lipase increases low density lipoprotein retention by subendothelial cell matrix.
pubmed:affiliation
Department of Medicine, Columbia University, College of Physicians and Surgeons, New York 10032.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't