Evidence map›Paper›PMID 21041949›Full record

ArticleThe Journal of clinical investigation2010

LXR promotes the maximal egress of monocyte-derived cells from mouse aortic plaques during atherosclerosis regression.

Jonathan E Feig, Ines Pineda-Torra, Marie Sanson, Michelle N Bradley, Yuliya Vengrenyuk, Dusan Bogunovic, Emmanuel L Gautier, Daniel Rubinstein, Cynthia Hong, Jianhua Liu and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
17.8field-weighted citation impact, top 1% 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

106 citing papers in PubMed, 186 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Is IDOL an Ideal Target for Treating Atherosclerosis?Arteriosclerosis, thrombosis, and vascular biology · 2025
    Article
  7. Article
  8. Review
  9. Article
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  11. Observational
  12. Review
  13. Article
  14. Review
  15. Article
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  17. Article
  18. Article
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46 more citing papers are in PubMed but not listed here.

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

16 authors at 5 institutions in 3 countries.

Jonathan E FeigDepartment of Medicine, Division of Cardiology, New York University School of Medicine, New York, New York, USA.
Ines Pineda-Torra
Marie Sanson
Michelle N Bradley
Yuliya Vengrenyuk
Dusan Bogunovic
Emmanuel L Gautier
Daniel Rubinstein
Cynthia Hong
Jianhua Liu
Chaowei Wu
Nico van Rooijen
Nina Bhardwaj
Michael Garabedian
Peter Tontonoz
Edward A Fisher
New York University · USUCLA Health · USHoward Hughes Medical Institute · USUnité de recherche sur les maladies cardiovasculaires et métaboliques · FRVrije Universiteit Amsterdam · NL

Funding

ULTRASTRUCTURE OF THE INTIMA IN EARLY LESION FORMATIONP01HL030568 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FOGELMAN, ALAN M · 1985 to 2019
$55.2M
Molecular Regulation of Atherosclerosis Regression - RenewalR01HL084312 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FISHER, EDWARD A · 2006 to 2024
$11.4M
Training Program in Cardiovascular SciencesT32HL098129 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Glenn I Fishman, Ira J Goldberg · 2009 to 2026
$5.9M
NUCLEAR RECEPTOR SIGNALING PATHWAYS IN ATHEROGENESISR01HL066088 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TONTONOZ, PETER J · 2001 to 2018
$5.4M
Role and Regulation of CCR7 in Regression of Atherosclerotic LesionsF30AG029748 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FEIG, JONATHAN E · 2007 to 2010
$170k
NHLBI NIH HHS HL-066088NHLBI NIH HHS HL-084312NHLBI NIH HHS HL-098129NHLBI NIH HHS P01 HL030568NHLBI NIH HHS R01 HL066088NHLBI NIH HHS R01 HL084312NHLBI NIH HHS T32 HL098129NIA NIH HHS AG-029748NIA NIH HHS F30 AG029748
6 · The paper itself

Abstract

We have previously shown that mouse atherosclerosis regression involves monocyte-derived (CD68+) cell emigration from plaques and is dependent on the chemokine receptor CCR7. Concurrent with regression, mRNA levels of the gene encoding LXRalpha are increased in plaque CD68+ cells, suggestive of a functional relationship between LXR and CCR7. To extend these results, atherosclerotic Apoe-/- mice sufficient or deficient in CCR7 were treated with an LXR agonist, resulting in a CCR7-dependent decrease in plaque CD68+ cells. To test the requirement for LXR for CCR7-dependent regression, we transplanted aortic arches from atherosclerotic Apoe-/- mice, or from Apoe-/- mice with BM deficiency of LXRalpha or LXRbeta, into WT recipients. Plaques from both LXRalpha and LXRbeta-deficient Apoe-/- mice exhibited impaired regression. In addition, the CD68+ cells displayed reduced emigration and CCR7 expression. Using an immature DC line, we found that LXR agonist treatment increased Ccr7 mRNA levels. This increase was blunted when LXRalpha and LXRbeta levels were reduced by siRNAs. Moreover, LXR agonist treatment of primary human immature DCs resulted in functionally significant upregulation of CCR7. We conclude that LXR is required for maximal effects on plaque CD68+ cell expression of CCR7 and monocyte-derived cell egress during atherosclerosis regression in mice.

Indexed as

AnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticAorta, ThoracicAtherosclerosisBenzenesulfonamidesCD68 MoleculeCell LineCell MovementDendritic CellsFemaleFluorocarbonsGene Expression RegulationHumansHydrocarbons, FluorinatedLiver X ReceptorsAntigens, CDAntigens, Differentiation, MyelomonocyticBenzenesulfonamidesCcr7 protein, mouseCD68 antigen, humanCD68 MoleculeFluorocarbonsHydrocarbons, FluorinatedLiver X ReceptorsNR1H3 protein, humanNr1h3 protein, mouseOrphan Nuclear ReceptorsReceptors, CCR7SulfonamidesT0901317

Identifiers

PMID21041949
PMCPMC2993578
OpenAlexW2143786800

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.