Evidence map›Paper›PMID 8690797›Full record

ArticleThe Journal of clinical investigation1996

Regulation of cellular proliferation and intimal formation following balloon injury in atherosclerotic rabbit arteries.

R D Simari, H San, M Rekhter, T Ohno, D Gordon, G J Nabel, E G Nabel

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

16 citing papers in PubMed, 101 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Nanoparticulate carriers for the treatment of coronary restenosis.International journal of nanomedicine · 2007
    Review
  7. Cardiovascular gene delivery: The good road is awaiting.Advanced drug delivery reviews · 2006
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Nonviral gene transfer strategies for the vasculature.Microcirculation (New York, N.Y. : 1994) · 2002
    Review
  13. Article
  14. Article
  15. Article
  16. 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

7 authors at 2 institutions in 2 countries.

R D SimariDepartment of Internal Medicine, University of Michigan, Ann Arbor 48109, USA.
H San
M Rekhter
T Ohno
D Gordon
G J Nabel
E G Nabel
University of Michigan–Ann Arbor · USHoward Hughes Medical Institute · US

Funding

SLC and dendritic cells in antitumor immunity &therapyP01CA059327 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHANG, ALFRED E · 1992 to 2005
$8.2M
PROLIFERATION AND GROWTH FACTORS IN ATHEROSCLEROSISR01HL042119 · NHLBI · UNIVERSITY OF WASHINGTON · PI GORDON, DAVID · 1989 to 1997
–
EXPRESSION AND BIOLOGICAL FUNCTION OF RECOMBINANT PDGFR01HL043757 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NABEL, ELIZABETH G · 1992 to 1995
–
NCI NIH HHS CA59327NHLBI NIH HHS HL42119NHLBI NIH HHS HL43757
6 · The paper itself

Abstract

Injury to atherosclerotic arteries induces the expression of growth regulatory genes that stimulate cellular proliferation and intimal formation. Intimal expansion has been reduced in vivo in nonatherosclerotic balloon-injured arteries by transfer of genes that inhibit cell proliferation. It is not known, however, whether vascular cell proliferation can be inhibited after injury in more extensively diseased atherosclerotic arteries. Accordingly, the purpose of this study was to investigate whether expression of recombinant genes in atherosclerotic arteries after balloon injury could inhibit intimal cell proliferation. To test this hypothesis, we examined the response to balloon injury in atherosclerotic rabbit arteries after gene transfer of herpesvirus thymidine kinase gene (tk) and administration of ganciclovir. Smooth muscle cells from hyperlipidemic rabbit arteries infected with adenoviral vectors encoding tk were sensitive to ganciclovir, and bystander killing was observed in vitro. In atherosclerotic arteries, a human placental alkaline phosphatase reporter gene was expressed in intimal and medial smooth muscle cells and macrophages, identifying these cells as targets for gene transfer. Expression of tk in balloon-injured hyperlipidemic rabbit arteries followed by ganciclovir treatment resulted in a 64% reduction in intimal cell proliferation 7 d after gene transfer (P = 0.004), and a 35-49% reduction in internal area 21 d after gene transfer, compared with five different control groups (P < 0.05). Replication of smooth muscle cells and macrophages was inhibited by tk expression and ganciclovir treatment. These findings indicate that transfer of a gene that inhibits cellular proliferation limits the intimal area in balloon-injured atherosclerotic arteries. Molecular approaches to the inhibition of cell proliferation in atherosclerotic arteries constitute a possible treatment for vascular proliferative diseases.

Indexed as

Gene Transfer TechniquesAdenoviridaeAnimalsAntiviral AgentsArteriesArteriosclerosisCatheterizationCell CycleGanciclovirGene ExpressionGenes, ReporterHerpesviridaeHumansMuscle DevelopmentMuscle, Smooth, VascularRabbitsAntiviral AgentsGanciclovirThymidine Kinase

Identifiers

PMID8690797
PMCPMC507420
OpenAlexW2035813375

What OpenQuestion holds

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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.