Evidence map›Paper›PMID 24212237›Full record

ArticleJournal of lipid research2014

ABCG1-mediated generation of extracellular cholesterol microdomains.

Sebastian R Freeman, Xueting Jin, Joshua J Anzinger, Qing Xu, Sonya Purushothaman, Michael B Fessler, Lia Addadi, Howard S Kruth

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  3. Review
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  7. 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
  8. Article
  9. Article
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  12. Macrophages release plasma membrane-derived particles rich in accessible cholesterol.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  13. Two polymorphic cholesterol monohydrate crystal structures form in macrophage culture models of atherosclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  14. Article
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  18. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

Sebastian R FreemanSection of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
Xueting Jin
Joshua J Anzinger
Qing Xu
Sonya Purushothaman
Michael B Fessler
Lia Addadi
Howard S Kruth
National Heart Lung and Blood Institute · USNational Institutes of Health · USNational Institute of Environmental Health Sciences · USWeizmann Institute of Science · IL

Funding

Cell Signaling of Host DefenseZIAES102005 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI FESSLER, MICHAEL B · 2009 to 2025
$41.7M
Mechanism Of Cholesterol Accumulation In Human AtherosclerosisZIAHL002832 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI KRUTH, HOWARD S · 2009 to 2019
$12.3M
Intramural NIH HHS
6 · The paper itself

Abstract

Previous studies have demonstrated that the ATP-binding cassette transporters (ABC)A1 and ABCG1 function in many aspects of cholesterol efflux from macrophages. In this current study, we continued our investigation of extracellular cholesterol microdomains that form during enrichment of macrophages with cholesterol. Human monocyte-derived macrophages and mouse bone marrow-derived macrophages, differentiated with macrophage colony-stimulating factor (M-CSF) or granulocyte macrophage colony-stimulation factor (GM-CSF), were incubated with acetylated LDL (AcLDL) to allow for cholesterol enrichment and processing. We utilized an anti-cholesterol microdomain monoclonal antibody to reveal pools of unesterified cholesterol, which were found both in the extracellular matrix and associated with the cell surface, that we show function in reverse cholesterol transport. Coincubation of AcLDL with 50 μg/ml apoA-I eliminated all extracellular and cell surface-associated cholesterol microdomains, while coincubation with the same concentration of HDL only removed extracellular matrix-associated cholesterol microdomains. Only at an HDL concentration of 200 µg/ml did HDL eliminate the cholesterol microdomains that were cell-surface associated. The deposition of cholesterol microdomains was inhibited by probucol, but it was increased by the liver X receptor (LXR) agonist TO901317, which upregulates ABCA1 and ABCG1. Extracellular cholesterol microdomains did not develop when ABCG1-deficient mouse bone marrow-derived macrophages were enriched with cholesterol. Our findings show that generation of extracellular cholesterol microdomains is mediated by ABCG1 and that reverse cholesterol transport occurs not only at the cell surface but also within the extracellular space.

Indexed as

AnimalsAnticholesteremic AgentsApolipoprotein A-IATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 1BenzenesulfonamidesCells, CulturedCholesterolFluorocarbonsHumansHydrocarbons, FluorinatedLipid MetabolismLipoproteins, HDLLiver X ReceptorsMacrophagesMaleABCG1 protein, humanAnticholesteremic AgentsApolipoprotein A-IATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 1BenzenesulfonamidesCholesterolFluorocarbonsHydrocarbons, FluorinatedLipoproteins, HDLLiver X ReceptorsOrphan Nuclear ReceptorsProbucolSulfonamidesT0901317apolipoprotein A-Iatherosclerosishigh density lipoproteinmacrophagesprobucol

Identifiers

PMID24212237
PMCPMC3927477
OpenAlexW2062965852

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.