Evidence map›Paper›PMID 22053073›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2012

ApoE suppresses atherosclerosis by reducing lipid accumulation in circulating monocytes and the expression of inflammatory molecules on monocytes and vascular endothelium.

Nathalie Gaudreault, Nikit Kumar, Jessica M Posada, Kyle B Stephens, Nabora Soledad Reyes de Mochel, Delphine Eberlé, Victor R Olivas, Roy Y Kim, Matthew J Harms, Sean Johnson and 3 more

Abstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

38 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. SR-B1-/-ApoE-R61h/h Mice Mimic Human Coronary Heart Disease.Cardiovascular drugs and therapy · 2024
    Review
  6. Observational
  7. Article
  8. Article
  9. IL-4 polarized human macrophage exosomes control cardiometabolic inflammation and diabetes in obesity.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. NLRP3 inflammasome promotes diabetes-induced endothelial inflammation and atherosclerosis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019
    Article
  18. Review
  19. Cell-specific production, secretion, and function of apolipoprotein E.Journal of molecular medicine (Berlin, Germany) · 2018
    Review
  20. Isolation of Plasma Lipoproteins as a Source of Extracellular RNA.Methods in molecular biology (Clifton, N.J.) · 2018
    Article
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

13 authors at 1 institution in 1 country.

Nathalie GaudreaultDepartment of Surgery, University of California San Francisco and VA Medical Center, 4150 Clement Street, San Francisco, CA 94121, USA.
Nikit Kumar
Jessica M Posada
Kyle B Stephens
Nabora Soledad Reyes de Mochel
Delphine Eberlé
Victor R Olivas
Roy Y Kim
Matthew J Harms
Sean Johnson
Louis M Messina
Joseph H Rapp
Robert L Raffai
University of Massachusetts Chan Medical School · US

Funding

Role of apolipoprotein E4 in the progression and regression of atherosclerosisR01HL089871 · NHLBI · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI RAFFAI, ROBERT · 2007 to 2011
$2.2M
Does Diabetic Hyperglycemia Regulate Atherosclerosis Progression and Regression?I01BX000532 · VA · VETERANS AFFAIRS MED CTR SAN FRANCISCO · PI RAFFAI, ROBERT · 2009 to 2013
–
BLRD VA I01 BX000532NHLBI NIH HHS HL089871NHLBI NIH HHS R01 HL089871
6 · The paper itself

Abstract

objectiveWe investigated atheroprotective properties of apolipoprotein (apo) E beyond its ability to lower plasma cholesterol. We hypothesized that apoE reduces atherosclerosis by decreasing lipid accumulation in circulating monocytes and the inflammatory state of monocytes and the vascular endothelium. METHODS AND

resultsWe developed mice with spontaneous hyperlipidemia with and without plasma apoE. Hypomorphic apoE mice deficient in low-density lipoprotein receptor (Apoe(h/h)Ldlr(-/-)) were compared to Apoe(-/-)Ldlr(-/-) mice. Despite 4-fold more plasma apoE than WT mice, Apoe(h/h)Ldlr(-/-) mice displayed similar plasma cholesterol as Apoe(-/-) Ldlr(-/-) mice but developed 4-fold less atherosclerotic lesions by 5 months of age. The aortic arch of Apoe(h/h)Ldlr(-/-) mice showed decreased endothelial expression of ICAM-1, PECAM-1, and JAM-A. In addition, Apoe(h/h)Ldlr(-/-) mice had less circulating leukocytes and proinflammatory Ly6C(high) monocytes. These monocytes had decreased neutral lipid content and reduced surface expression of ICAM-1, VLA-4, and L-Selectin. Apoe(h/h)Ldlr(-/-) mice displayed increased levels of apoA1-rich HDL that were potent in promoting cellular cholesterol efflux.

conclusionsOur findings suggest that apoE reduces atherosclerosis in the setting of hyperlipidemia by increasing plasma apoA1-HDL that likely contribute to reduce intracellular lipid accumulation and thereby the activation of circulating leukocytes and the vascular endothelium.

Indexed as

Lipid MetabolismAnimalsApolipoproteins EAtherosclerosisCell Adhesion MoleculesCholesterolDisease Models, AnimalEndothelium, VascularInflammation MediatorsIntegrin alpha4beta1Intercellular Adhesion Molecule-1L-SelectinMiceMice, Inbred C57BLMice, KnockoutMonocytesApolipoproteins ECell Adhesion MoleculesCholesterolF11r protein, mouseInflammation MediatorsIntegrin alpha4beta1Intercellular Adhesion Molecule-1L-SelectinPlatelet Endothelial Cell Adhesion Molecule-1Receptors, Cell SurfaceReceptors, LDL

Identifiers

PMID22053073
PMCPMC3275345
OpenAlexW2138026874

What OpenQuestion holds

Textmetadata
LicenceTDM
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.