Evidence map›Paper›PMID 23686114›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2013

Differential regulation of gene expression by LXRs in response to macrophage cholesterol loading.

Irena D Ignatova, Jerry Angdisen, Erin Moran, Ira G Schulman

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2013. 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
2.3field-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, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Liver X receptors and liver physiology.Biochimica et biophysica acta. Molecular basis of disease · 2021
    Review
  6. 27-Hydroxycholesterol induces macrophage gene expressionThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021
    Article
  7. Article
  8. Article
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  10. Article
  11. Review
  12. Article
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  15. Article
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  17. Review
  18. 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

4 authors at 1 institution in 1 country.

Irena D IgnatovaDepartment of Pharmacology, University of Virginia, 1300 Jefferson Park Avenue, PO Box 800735, Charlottesville, Virginia 22908, USA. igs4c@virginia.edu
Jerry Angdisen
Erin Moran
Ira G Schulman
University of Virginia Health System · US

Funding

Women's Oncology Program - WONP30CA044579 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Thomas P. Loughran · 1987 to 2026
$72.1M
Subtype Specific LXR Activity Limits AtherosclerosisR01HL096864 · NHLBI · UNIVERSITY OF VIRGINIA · PI SCHULMAN, IRA G · 2010 to 2013
$1.5M
NCI NIH HHS P30 CA044579NHLBI NIH HHS 1R01HL096864NHLBI NIH HHS R01 HL096864
6 · The paper itself

Abstract

The ability of cells to precisely control gene expression in response to intracellular and extracellular signals plays an important role in both normal physiology and in pathological settings. For instance, the accumulation of excess cholesterol by macrophages initiates a genetic response mediated by the liver X receptors (LXRs)-α (NR1H3) and LXRβ (NR1H2), which facilitates the transport of cholesterol out of cells to high-density lipoprotein particles. Studies using synthetic LXR agonists have also demonstrated that macrophage LXR activation simultaneously induces a second network of genes that promotes fatty acid and triglyceride synthesis that may support the detoxification of excess free cholesterol by storage in the ester form. We now show that treatment of human THP-1 macrophages with endogenous or synthetic LXR ligands stimulates both transcriptional and posttranscriptional pathways that result in the selective recruitment of the LXRα subtype to LXR-regulated promoters. Interestingly, when human or mouse macrophages are loaded with cholesterol under conditions that mimic the development of atherogenic macrophage foam cells, a selective LXR response is generated that induces genes mediating cholesterol transport but does not coordinately regulate genes involved in fatty acid synthesis. The gene-selective response to cholesterol loading occurs, even in the presence of LXRα binding to the promoter of the gene encoding the sterol regulatory element-binding protein-1c, the master transcriptional regulator of fatty acid synthesis. The ability of promoter bound LXRα to recruit RNA polymerase to the sterol regulatory element-binding protein-1c promoter, however, appears to be ligand selective.

Indexed as

AnimalsATP Binding Cassette Transporter 1Cell LineCholesterolGene Expression RegulationHalf-LifeHumansLigandsLiver X ReceptorsMacrophagesMiceOrphan Nuclear ReceptorsPromoter Regions, GeneticProtein BindingResponse ElementsSterol Regulatory Element Binding Protein 1ABCA1 protein, humanATP Binding Cassette Transporter 1CholesterolLigandsLiver X ReceptorsNR1H2 protein, humanNr1h2 protein, mouseNR1H3 protein, humanNr1h3 protein, mouseOrphan Nuclear ReceptorsSterol Regulatory Element Binding Protein 1

Identifiers

PMID23686114
PMCPMC3706843
OpenAlexW2026516154

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.