Evidence map›Paper›PMID 22914792›Full record

ArticleHypertension (Dallas, Tex. : 1979)2012

Apolipoprotein E enhances endothelial-NO production by modulating caveolin 1 interaction with endothelial NO synthase.

Lili Yue, Jing-Tan Bian, Ivana Grizelj, Ana Cavka, Shane A Phillips, Ayako Makino, Theodore Mazzone

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Review
  3. Genes · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Apolipoprotein E in Cardiometabolic and Neurological Health and Diseases.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Role of Caveolin-1 in Diabetes and Its Complications.Oxidative medicine and cellular longevity · 2020
    Review
  17. Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Lili YueDepartment of Medicine, University of Illinois at Chicago, Chicago, IL, USA.
Jing-Tan Bian
Ivana Grizelj
Ana Cavka
Shane A Phillips
Ayako Makino
Theodore Mazzone
University of Illinois Chicago · US

Funding

Effects of Low Carbohydrate and Low Fat Diets on Endothelium Function in ObesityR01HL095701 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI PHILLIPS, SHANE A · 2010 to 2014
$2.1M
Adipocyte Lipid Metabolism and ApoE ExpressionR01DK071711 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MAZZONE, THEODORE · 2006 to 2009
$1.2M
Mechanisms of exertional hypertension and vascular dysfunctionK23HL085614 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI PHILLIPS, SHANE A · 2007 to 2011
$645k
Mechanisms of coronary endothelial dysfunction in diabetesK01DK083506 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MAKINO, AYAKO · 2009 to 2011
$366k
Adipocyte Lipid Metabolism and ApoE ExpressionR56DK071711 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MAZZONE, THEODORE · 2005 to 2010
$352k
Advanced Software for Enabling Quantitative 3D Stress EchocardiographyR41HL095201 · NHLBI · IGI TECHNOLOGIES, INC. · PI PLISHKER, WILLIAM LESTER · 2009 to 2009
$100k
NHLBI NIH HHS HL 095201NHLBI NIH HHS HL 85614NHLBI NIH HHS K23 HL085614NHLBI NIH HHS R01 HL095701NHLBI NIH HHS R41 HL095201NIDDK NIH HHS DK 083506NIDDK NIH HHS DK 71711NIDDK NIH HHS K01 DK083506NIDDK NIH HHS R01 DK071711NIDDK NIH HHS R56 DK071711
6 · The paper itself

Abstract

Apolipoprotein E (apoE) is widely expressed in mammalian tissues, and one of the important tissue-specific effects is the atheroprotection ascribed to macrophage-derived apoE in the arterial wall. However, underlying mechanisms are not well understood. In this study, using subcellular fractionation, confocal microscopy, and coimmunoprecipitation, we demonstrated that macrophage-derived apoE is internalized by endothelial cells and impacts the subcellular distribution/interaction of caveolin 1 (cav-1) and endothelial NO synthase (eNOS). The addition of apoE disrupts the heteromeric complex formed between cav-1 and eNOS, and increases NO production. Sterol and oxysterol enhance endothelial cav-1/eNOS interaction and suppress NO production, but these effects are reversed by apoE. Silencing endothelial cav-1 attenuates apoE-induced NO production, establishing the importance of the cav-1-eNOS interaction for the increment in endothelial NO produced by apoE. Consistent with these observations, macrophage-derived apoE significantly improves vasodilation to acetylcholine in resistance arteries isolated from adipose tissue of obese humans. We conclude that macrophage-derived apoE enhances endothelial NO production by disrupting the inhibitory interaction of eNOS with cav-1. These results establish a novel mechanism by which apoE modulates endothelial cell function.

Indexed as

AnimalsApolipoproteins ECaveolin 1Endothelial CellsFemaleHumansHuman Umbilical Vein Endothelial CellsIntra-Abdominal FatMacrophagesMaleMiceMice, KnockoutNitric OxideNitric Oxide Synthase Type IIIApolipoproteins ECaveolin 1Nitric OxideNitric Oxide Synthase Type III

Identifiers

PMID22914792
PMCPMC3740794
OpenAlexW2108555467

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.