Evidence map›Paper›PMID 21772254›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2011

Expression of apolipoprotein A-I in rabbit carotid endothelium protects against atherosclerosis.

Rowan Flynn, Kun Qian, Chongren Tang, Nagadhara Dronadula, Joshua M Buckler, Bo Jiang, Shan Wen, Helén L Dichek, David A Dichek

Open access · bronzeAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2011. 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
1.8field-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

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Apolipoprotein A-I vascular gene therapy reduces vein-graft atherosclerosis.Molecular therapy. Methods & clinical development · 2023
    Article
  4. Article
  5. Review
  6. ABCA1, ABCG1, and Cholesterol Homeostasis.Advances in experimental medicine and biology · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. In Vivo Gene Transfer to the Rabbit Common Carotid Artery Endothelium.Journal of visualized experiments : JoVE · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Helper-Dependent Adenoviral Vectors.Journal of genetic syndromes & gene therapy · 2011
    Article
  20. Review
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

9 authors at 1 institution in 1 country.

Rowan FlynnDepartment of Medicine, University of Washington, Seattle, Washington 98195-7710, USA.
Kun Qian
Chongren Tang
Nagadhara Dronadula
Joshua M Buckler
Bo Jiang
Shan Wen
Helén L Dichek
David A Dichek
University of Washington · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Sakeneh Zraika · 1986 to 2026
$41.4M
CARDIOVASCULAR RESEARCH TRAINING PROGRAMT32HL007828 · NHLBI · UNIVERSITY OF WASHINGTON · PI Francis Kim, Farid Moussavi-Harami · 1997 to 2026
$10.2M
Engineering Blood Vessels to Resist AtherosclerosisR01HL076226 · NHLBI · UNIVERSITY OF WASHINGTON · PI DICHEK, DAVID A · 2006 to 2009
$2.1M
NHLBI NIH HHS HL076226NHLBI NIH HHS R01 HL076226NHLBI NIH HHS T32 HL007828NHLBI NIH HHS T32HL007828NIDDK NIH HHS P30 DK017047NIDDK NIH HHS P30DK017047
6 · The paper itself

Abstract

Expression of atheroprotective genes in the blood vessel wall is potentially an effective means of preventing or reversing atherosclerosis. Development of this approach has been hampered by lack of a suitable gene-transfer vector. We used a helper-dependent adenoviral (HDAd) vector to test whether expression of apolipoprotein A-I (apoA-I) in the artery wall could retard the development of atherosclerosis in hyperlipidemic rabbits. Carotid arteries were infused with an HDAd expressing rabbit apoA-I or a "null" HDAd and harvested 2 and 4 weeks later. ApoA-I mRNA and protein were detected only in HDAdApoAI arteries. Lesion size, lipid and macrophage content, and adhesion molecule expression were similar in both groups at 2 weeks. Between 2 and 4 weeks, most of these measures of atherosclerosis increased in HDAdNull arteries, but were stable or decreased in HDAdApoAI arteries (P ≤ 0.04 for all end points in 4-week HDAdApoAI versus HDAdNull arteries). A longer-term study in chow-fed rabbits revealed persistence of HDAd vector DNA and apoA-I expression for ≥48 weeks, with stable vector DNA content and apoA-I expression from 4 to 48 weeks. Expression of apoA-I in arterial endothelium significantly retards atherosclerosis. HDAd provides prolonged, stable expression of a therapeutic transgene in the artery wall.

Indexed as

AnimalsApolipoprotein A-IAtherosclerosisCarotid ArteriesCholesterolEndothelium, VascularMacrophagesMiceMice, KnockoutRabbitsRNA, MessengerTunica IntimaApolipoprotein A-ICholesterolRNA, Messenger

Identifiers

PMID21772254
PMCPMC3188740
OpenAlexW1969402966

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.