Evidence map›Paper›PMID 20808287›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2010

Helper-dependent adenoviral vectors are superior in vitro to first-generation vectors for endothelial cell-targeted gene therapy.

Rowan Flynn, Joshua M Buckler, Chongren Tang, Francis Kim, David A Dichek

Open access · hybridAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2010. 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
1.3field-weighted citation impact, top 18% 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, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Inhibition of miR-33a-5p in Macrophage-like Cells In Vitro Promotes apoAI-Mediated Cholesterol Efflux.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024
    Article
  5. Apolipoprotein A-I vascular gene therapy reduces vein-graft atherosclerosis.Molecular therapy. Methods & clinical development · 2023
    Article
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  18. Helper-Dependent Adenoviral Vectors.Journal of genetic syndromes & gene therapy · 2011
    Article
  19. Expression of apolipoprotein A-I in rabbit carotid endothelium protects against atherosclerosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2011
    Article
  20. 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

5 authors at 1 institution in 1 country.

Rowan FlynnDepartment of Medicine, University of Washington, Seattle, Washington, USA.
Joshua M Buckler
Chongren Tang
Francis Kim
David A Dichek
University of Washington · US

Funding

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 HL076226
6 · The paper itself

Abstract

Arterial endothelial cells (EC) are attractive targets for gene therapy of atherosclerosis because they are accessible to hematogenous and catheter-based vector delivery and overlie atherosclerotic plaques. Vector-mediated expression-in EC-of proteins that mediate cholesterol transfer out of the artery wall and decrease inflammation could prevent and reverse atherosclerosis. However, clinical application of this strategy is limited by lack of a suitable gene-transfer vector. First-generation adenovirus (FGAd) is useful for EC gene transfer in proof-of-concept studies, but is unsuitable for atheroprotective human gene therapy because of limited duration of expression and proinflammatory effects. Moreover, others have reported detrimental effects of FGAd on critical aspects of EC physiology including proliferation, migration, and apoptosis. Here, we investigated whether helper-dependent adenovirus (HDAd) either alone or expressing an atheroprotective gene [apolipoprotein A-I (apoA-I)] could circumvent these limitations. In contrast to control FGAd, HDAd did not alter any of several critical EC physiologic functions (including proliferation, migration, apoptosis, metabolic activity, and nitric oxide (NO) production) and did not stimulate proinflammatory pathways [including expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and interleukin-6 (IL-6)]. Expression of apoA-I by HDAd reduced EC VCAM-1 expression. HDAd is a promising vector and apoA-I is a promising gene for atheroprotective human gene therapy delivered via EC.

Indexed as

Drug Delivery SystemsGenetic TherapyGenetic VectorsAdenoviridaeAnimalsAntigens, CDAortaApolipoprotein A-ICattleCell Adhesion MoleculesEndothelial CellsHumansNitric OxideAntigens, CDApolipoprotein A-ICell Adhesion MoleculesICAM2 protein, humanNitric Oxide

Identifiers

PMID20808287
PMCPMC2997586
OpenAlexW1997466549

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.