| Apolipoprotein A-I promotes cholesterol release and apolipoprotein E recruitment from THP-1 macrophage-like foam cells. | |
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MedLine Citation:
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PMID: 9869653 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Apolipoprotein E (apoE) is synthesized and secreted by arterial macrophages while apolipoprotein A-I (apoA-I) is present in surrounding interstitial fluids. Both apolipoproteins play important roles in macrophage cholesterol homeostasis by forming lipid complexes (nascent-HDL) with cellular phospholipids (PL) and cholesterol (UC) thereby promoting cholesterol efflux. In this study, we evaluated the relative contributions of apoA-I and endogenously produced apoE in mediating the recruitment of cellular cholesterol. THP-1 human monocytes were differentiated (300 nm phorbol dibutyrate) into macrophages and macrophage-foam cells were generated by cholesterol loading with acetylated LDL (50 microg protein/ml). ApoA-I (10 microg/ml) depleted macrophage-foam cell cholesteryl esters by 50% in 24 h. This reduction was accompanied by a significant increase in the UC/PL mole ratio of nascent HDL (UC/PL = 0.80 +/- 0.15) in the medium compared to complexes isolated from macrophages (UC/PL = 0.59 +/- 0.08). Significantly more (70%) nascent-HDL were formed in incubations of apoA-I with macrophage-foam cells than with macrophages. Medium apoE accumulation paralleled the assembly of apoA-I containing nascent HDL where 2- and 4-fold increases were observed with macrophages and macrophage-foam cells, respectively, compared to incubations in the absence of apoA-I. Despite the increase in medium apoE accumulation, a majority (85%) of particles (11, 9, and 7.4 nm in diameter) from macrophages and macrophage-foam cells possessed apoA-I without apoE. ApoA-I plus apoE particles (13-16 nm) were also formed along with a small quantity of apoE-only particles (19-20 nm). The predominance of apoA-I only particles indicates, however, that the assembly of apoA-I-containing nascent-HDL represents a major metabolic pathway of cellular cholesterol recruitment compared to the endogenous production of apoE. |
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Authors:
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J K Bielicki; M R McCall; T M Forte |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of lipid research Volume: 40 ISSN: 0022-2275 ISO Abbreviation: J. Lipid Res. Publication Date: 1999 Jan |
Date Detail:
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Created Date: 1999-03-09 Completed Date: 1999-03-09 Revised Date: 2009-11-03 |
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: 85-92 Citation Subset: IM |
Affiliation:
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Ernest Orlando Lawrence Berkeley National Laboratory, Life Sciences Division 1-213, University of California, Berkeley CA 94720, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Apolipoprotein A-I
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metabolism,
pharmacology* Apolipoproteins E / metabolism* Cell Differentiation Cell Line Cholesterol / metabolism* Cholesterol Esters / metabolism Culture Media, Conditioned Foam Cells / cytology, drug effects*, metabolism* Humans Lipoproteins, HDL / chemistry, metabolism Monocytes / cytology, drug effects, metabolism Particle Size Phospholipids / analysis, classification, metabolism |
| Grant Support | |
ID/Acronym/Agency:
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HL 18574/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Apolipoprotein A-I; 0/Apolipoproteins E; 0/Cholesterol Esters; 0/Culture Media, Conditioned; 0/Lipoproteins, HDL; 0/Phospholipids; 57-88-5/Cholesterol |
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