Evidence map›Paper›PMID 20421591›Full record

ArticleJournal of lipid research2010

Extracellular cholesterol-rich microdomains generated by human macrophages and their potential function in reverse cholesterol transport.

Daniel S Ong, Joshua J Anzinger, Francisco J Leyva, Noa Rubin, Lia Addadi, Howard S Kruth

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2010. 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
2.4field-weighted citation impact, top 12% 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, 36 citations in OpenAlex.

  1. Review
  2. Different Pathways of Cellular Cholesterol Efflux.Cell biochemistry and biophysics · 2022
    Review
  3. Examining atherosclerotic lesions in three dimensions at the nanometer scale with cryo-FIB-SEM.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  4. Article
  5. A new pathway of macrophage cholesterol efflux.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  6. 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
  7. Article
  8. Article
  9. Review
  10. 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
  11. 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
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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

6 authors at 3 institutions in 2 countries.

Daniel S OngSection of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1422, USA.
Joshua J Anzinger
Francisco J Leyva
Noa Rubin
Lia Addadi
Howard S Kruth
National Heart Lung and Blood Institute · USWeizmann Institute of Science · ILNational Institutes of Health · US

Funding

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

Previous studies have shown that cholesterol in atherosclerotic plaques is present in both intracellular and extracellular forms. In the current study, we investigated a mechanism for extracellular cholesterol accumulation and examined the capacity of this pool of cholesterol to be removed by cholesterol acceptors, a step in reverse cholesterol transport. Human monocyte-derived macrophages differentiated with macrophage-colony stimulating factor were incubated with acetylated LDL to allow cholesterol enrichment and processing. These macrophages were subsequently labeled with a monoclonal antibody that specifically detects ordered cholesterol arrays, revealing the presence of unesterified cholesterol-rich microdomains on the cell surfaces and in the extracellular matrix. Similar unesterified cholesterol-rich microdomains were present in human atherosclerotic plaques. Actin microfilaments functioned in microdomain deposition or maintenance, and Src family kinases regulated transfer of these microdomains from the cell surface onto the extracellular matrix. Mediators of reverse cholesterol transport, apolipoprotein A-I (apoA-I), and HDL were capable of removing these extracellular un-esterified cholesterol-rich microdomains. However, apoA-I removed the microdomains only when macrophages were present. ApoA-I removal of microdomains was blocked by glyburide and inhibitor of ATP-binding cassette transporter A1 (ABCA1) function. In summary, cultures of cholesterol-enriched human monocyte-derived macrophages generate extracellular unesterified cholesterol-rich microdomains, which can subsequently be removed by cholesterol acceptors and therefore potentially function in reverse cholesterol transport.

Indexed as

AntibodiesAortaApolipoprotein A-IBiological TransportCell DifferentiationCells, CulturedCholesterolCytoskeletonEsterificationExtracellular SpaceGlyburideHumansLipoproteins, HDLMacrophage Colony-Stimulating FactorMacrophagesMembrane MicrodomainsAntibodiesApolipoprotein A-ICholesterolGlyburideLipoproteins, HDLMacrophage Colony-Stimulating Factorsrc-Family Kinases

Identifiers

PMID20421591
PMCPMC2903806
OpenAlexW2118180586

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.