Evidence map›Paper›PMID 26203076›Full record

ArticleJournal of lipid research2015

ABCA1 contributes to macrophage deposition of extracellular cholesterol.

Xueting Jin, Sebastian R Freeman, Boris Vaisman, Ying Liu, Janet Chang, Neta Varsano, Lia Addadi, Alan Remaley, Howard S Kruth

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 22 citations in OpenAlex.

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  10. Cultured macrophages transfer surplus cholesterol into adjacent cells in the absence of serum or high-density lipoproteins.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
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  13. Macrophages release plasma membrane-derived particles rich in accessible cholesterol.Proceedings of the National Academy of Sciences of the United States of America · 2018
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Xueting JinSection of Experimental Atherosclerosis National Institutes of Health, Bethesda, MD 20892.
Sebastian R FreemanSection of Experimental Atherosclerosis National Institutes of Health, Bethesda, MD 20892.
Boris VaismanLipoprotein Metabolism Section, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Ying LiuSection of Experimental Atherosclerosis National Institutes of Health, Bethesda, MD 20892.
Janet ChangSection of Experimental Atherosclerosis National Institutes of Health, Bethesda, MD 20892.
Neta VarsanoDepartment of Structural Biology, Weizmann Institute of Science, 76100 Rehovot, Israel.
Lia AddadiDepartment of Structural Biology, Weizmann Institute of Science, 76100 Rehovot, Israel.
Alan RemaleyLipoprotein Metabolism Section, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Howard S KruthSection of Experimental Atherosclerosis National Institutes of Health, Bethesda, MD 20892.
National Institutes of Health · USWeizmann Institute of Science · ILNational Heart Lung and Blood Institute · US

Funding

NHLBI Animal Program DivisionZIGHL006020 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI CLARK, TANNIA · 2009 to 2025
$47.3M
Mechanism Of Cholesterol Accumulation In Human AtherosclerosisZIAHL002832 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI KRUTH, HOWARD S · 2009 to 2019
$12.3M
6 · The paper itself

Abstract

We previously reported that cholesterol-enriched macrophages excrete cholesterol into the extracellular matrix. A monoclonal antibody that detects cholesterol microdomains labels the deposited extracellular particles. Macro-phage deposition of extracellular cholesterol depends, in part, on ABCG1, and this cholesterol can be mobilized by HDL components of the reverse cholesterol transport process. The objective of the current study was to determine whether ABCA1 also contributes to macrophage deposition of extracellular cholesterol. ABCA1 functioned in extracellular cholesterol deposition. The liver X receptor agonist, TO901317 (TO9), an ABCA1-inducing factor, restored cholesterol deposition that was absent in cholesterol-enriched ABCG1(-/-) mouse macrophages. In addition, the ABCA1 inhibitor, probucol, blocked the increment in cholesterol deposited by TO9-treated wild-type macrophages, and completely inhibited deposition from TO9-treated ABCG1(-/-) macrophages. Lastly, ABCA1(-/-) macrophages deposited much less extracellular cholesterol than wild-type macrophages. These findings demonstrate a novel function of ABCA1 in contributing to macrophage export of cholesterol into the extracellular matrix.

Indexed as

AnimalsApolipoprotein A-IAtherosclerosisATP Binding Cassette Transporter 1ATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 1BenzenesulfonamidesCholesterolExtracellular MatrixFluorocarbonsHumansHydrocarbons, FluorinatedLipoproteinsLipoproteins, HDLLiver X ReceptorsMacrophagesAbca1 protein, mouseABCG1 protein, mouseApolipoprotein A-IATP Binding Cassette Transporter 1ATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 1BenzenesulfonamidesCholesterolFluorocarbonsHydrocarbons, FluorinatedLipoproteinsLipoproteins, HDLLiver X ReceptorsOrphan Nuclear ReceptorsProbucolSulfonamidesT0901317apolipoprotein A-IatherosclerosisATP binding cassette transporter A1ATP binding cassette transporter G1high density lipoproteinprobucolTO901317

Identifiers

PMID26203076
PMCPMC4548776
OpenAlexW2125632461

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.