Evidence map›Paper›PMID 7593602›Full record

ArticleThe Journal of clinical investigation1995

Macrophage-specific expression of human apolipoprotein E reduces atherosclerosis in hypercholesterolemic apolipoprotein E-null mice.

S Bellosta, R W Mahley, D A Sanan, J Murata, D L Newland, J M Taylor, R E Pitas

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

81 citing papers in PubMed, 282 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Endothelial CellArteriosclerosis, thrombosis, and vascular biology · 2023
    Article
  7. Macrophage Phenotyping in Atherosclerosis by Proteomics.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Apolipoprotein E and Alzheimer's disease.Acta pharmaceutica Sinica. B · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Immune cell metabolism in autoimmunity.Clinical and experimental immunology · 2019
    Review
  16. Article
  17. Article
  18. Review
  19. Apoprotein E and Reverse Cholesterol Transport.International journal of molecular sciences · 2018
    Review
  20. Article

21 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

7 authors at 1 institution in 1 country.

S BellostaGladstone Institute of Cardiovascular Disease, University of California, San Francisco 94141-9100, USA.
R W Mahley
D A Sanan
J Murata
D L Newland
J M Taylor
R E Pitas
Gladstone Institutes · US

Funding

TRANSGENIC ANIMAL MODEL OF TYPE III HYPERLIPOPROTEINEMIAP01HL047660 · NHLBI · J. DAVID GLADSTONE INSTITUTES · PI TAYLOR, JOHN M · 1992 to 2001
$2.9M
NHLBI NIH HHS HL-47660
6 · The paper itself

Abstract

apoE deficiency causes hyperlipidemia and premature atherosclerosis. To determine if macrophage-specific expression of apoE would decrease the extent of atherosclerosis, we expressed human apoE in macrophages of apoE-null mice (apoE-/-) and assessed the effect on lipid accumulation in cells of the arterial wall. Macrophage-specific expression of human apoE in normal mice was obtained by use of the visna virus LTR. These animals were bred with apoE-/- mice to produce animals hemizygous for expression of human apoE in macrophages in the absence of murine apoE (apoE-/-,hTgE+/0). Low levels of human apoE mRNA were present in liver and spleen and high levels in lung and peritoneal macrophages. Human apoE was secreted by peritoneal macrophages and was detected in Kupffer cells of the liver. Human apoE in the plasma of apoE-/-,hTgE+/0 mice (n = 30) was inversely correlated (P < 0.005) with the plasma cholesterol concentration. After 15 wk on a normal chow diet, atherosclerosis was assessed in apoE-/-,hTgE+/0 animals and in apoE-/-,hTgE0/0 littermates matched for plasma cholesterol level (approximately 450 mg/dl) and lipoprotein profile. There was significantly less atherosclerosis in both the aortic sinus and in the proximal aorta (P < 0.0001) in the animals expressing the human apoE transgene. In apo-E-/-,hTgE+/0 animals, which had detectable atherosclerotic lesions, human apoE was detected in the secretory apparatus of macrophage-derived foam cells in the arterial wall. The data demonstrate that expression of apoE by macrophages is antiatherogenic even in the presence of high levels of atherogenic lipoproteins. The data suggest that apoE prevents atherosclerosis by promoting cholesterol efflux from cells of the arterial wall.

Indexed as

AnimalsApolipoproteins EArteriosclerosisCells, CulturedCholesterolFemaleFoam CellsGene ExpressionGene Transfer TechniquesHumansHypercholesterolemiaMacrophagesMaleMiceMice, TransgenicApolipoproteins ECholesterol

Identifiers

PMID7593602
PMCPMC185866
OpenAlexW2134010411

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.