| Serum paraoxonase: effect of the apolipoprotein composition of HDL and the acute phase response. | |
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MedLine Citation:
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PMID: 12562837 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Genetic variations of paraoxonase (PON) correlate with HDL cholesterol and apolipoprotein A-I (apoA-I), suggesting antiatherogenic properties. Atherosclerosis occurs naturally in humans and rabbits but not in mice. We compared variations of PON arylesterase activity (PON AEase, phenylacetate substrate) in humans, rabbits, and mice. In humans and rabbits, >95% of PON AEase is HDL associated. In mice, about 30% of PON AEase is lipid poor. In the absence of apoA-I in mice, total PON AEase is reduced and >60% is lipid poor. PON AEase level and distribution is restored in apoA-I-/- mice injected with adenoviruses encoding human apoA-I and in transgenic mice expressing human apoA-I at a steady-state level. Thus, while apoA-I is not required for the HDL association of PON AEase, induced variations in apoA-I correlate with changes in HDL-associated, but not lipid-poor, PON AEase. PON AEase associates only with apoA-I- or apoE-containing HDL but not VLDL. In the absence of both apoA-I and apoE, PON AEase is all-lipid-poor. PON AEase is displaced from HDL by ultracentrifugation and following incubation with serum amyloid A. Variations in the PON distribution between HDL and lipid-poor fractions may have important consequences in its antioxidant activity and in atherogenesis. |
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Authors:
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Veneracion G Cabana; Catherine A Reardon; Ning Feng; Sean Neath; John Lukens; Godfrey S Getz |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. Date: 2003-01-16 |
Journal Detail:
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Title: Journal of lipid research Volume: 44 ISSN: 0022-2275 ISO Abbreviation: J. Lipid Res. Publication Date: 2003 Apr |
Date Detail:
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Created Date: 2003-04-01 Completed Date: 2004-03-02 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0376606 Medline TA: J Lipid Res Country: United States |
Other Details:
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Languages: eng Pagination: 780-92 Citation Subset: IM |
Affiliation:
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Department of Pathology, The University of Chicago, IL 60637, USA. vcabana@midway.uchicago.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acute-Phase Reaction
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blood* Animals Apolipoprotein A-I / genetics, metabolism Apolipoproteins / analysis*, metabolism Apolipoproteins E / metabolism Arteriosclerosis / etiology Aryldialkylphosphatase / blood, metabolism* Humans Lipoproteins, HDL / analysis*, metabolism Mice Mice, Transgenic Protein Binding Rabbits |
| Grant Support | |
ID/Acronym/Agency:
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HL-57334/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Apolipoprotein A-I; 0/Apolipoproteins; 0/Apolipoproteins E; 0/Lipoproteins, HDL; EC 3.1.8.1/Aryldialkylphosphatase |
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