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rdf:type |
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lifeskim:mentions |
umls-concept:C0003250,
umls-concept:C0023823,
umls-concept:C0033684,
umls-concept:C0034493,
umls-concept:C0205349,
umls-concept:C0221198,
umls-concept:C0332120,
umls-concept:C0439660,
umls-concept:C0439851,
umls-concept:C1552596,
umls-concept:C1947931
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pubmed:issue |
5
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pubmed:dateCreated |
1989-12-15
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pubmed:abstractText |
Low density lipoproteins (LDL) that have been oxidatively modified have been implicated in the pathogenesis of atherosclerosis. Monoclonal antibodies were generated against oxidatively modified human low density lipoproteins (OxLDL); these antibodies reacted with OxLDL, but did not react with native LDL, either in an enzyme-linked immunosorbent assay (ELISA) or a Western blot analysis. The anti-OxLDL antibodies did react with other modified forms of LDL (eg, acetylated LDL, malondialdehyde-modified LDL, and cell-modified LDL) that were recognized by the scavenger receptor on macrophages. Single- and double-label immunofluorescence of atheromatous lesions from a Watanabe heritable hyperlipidemic (WHHL) rabbit demonstrated some colocalization of proteins detected by anti-LDL and anti-OxLDL antibodies. However, clearly there were also areas stained by the anti-OxLDL antibodies that did not stain with anti-LDL. Staining of the lesion by the anti-OxLDL antibody was abolished by adsorption of the antibody with OxLDL, but not by adsorption with LDL or bovine serum albumin. Arterial tissue from a control New Zealand White rabbit did not show staining with anti-LDL or anti-OxLDL antibodies. These observations suggest that OxLDL (or possibly other proteins recognized by the anti-OxLDL antibody) is present in atheromatous lesions of WHHL rabbits, and are consistent with oxidatively modified lipoproteins having a role in atherogenesis.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-14933036,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-218198,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-2424465,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-2455346,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-2465552,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-3005364,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-3028347,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-3196727,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-3323390,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-3475709,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-3478721,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-3598198,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-3767695,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-3777135,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-3813980,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-3861749,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-3862109,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-3907462,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-3944273,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-3954672,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-3973770,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-6183272,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-6273873,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-6311077,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-6415194,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-6466193,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-6501577,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-6587396,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-672633,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-6769124,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2683796-7381323
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0002-9440
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
135
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
815-25
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:2683796-Animals,
pubmed-meshheading:2683796-Antibodies, Monoclonal,
pubmed-meshheading:2683796-Aorta,
pubmed-meshheading:2683796-Arteriosclerosis,
pubmed-meshheading:2683796-Blotting, Western,
pubmed-meshheading:2683796-Fluorescent Antibody Technique,
pubmed-meshheading:2683796-Hyperlipidemias,
pubmed-meshheading:2683796-Immunosorbent Techniques,
pubmed-meshheading:2683796-Lipoproteins, LDL,
pubmed-meshheading:2683796-Oxidation-Reduction,
pubmed-meshheading:2683796-Rabbits
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pubmed:year |
1989
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pubmed:articleTitle |
Direct evidence for a protein recognized by a monoclonal antibody against oxidatively modified LDL in atherosclerotic lesions from a Watanabe heritable hyperlipidemic rabbit.
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pubmed:affiliation |
Department of Pathology, University of Washington, Seattle 98195.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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