Evidence map›Paper›PMID 9329968›Full record

ArticleThe Journal of clinical investigation1997

Inducible nitric oxide synthase suppresses the development of allograft arteriosclerosis.

L L Shears, N Kawaharada, E Tzeng, T R Billiar, S C Watkins, I Kovesdi, A Lizonova, S M Pham

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
15.8field-weighted citation impact, top 1% 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

23 citing papers in PubMed, 247 citations in OpenAlex.

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  10. Generation of NO by bystander human CD8 T cells augments allogeneic responses by inhibiting cytokine deprivation-induced cell death.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2009
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  14. Nitric oxide inhibits exocytosis of cytolytic granules from lymphokine-activated killer cells.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
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  16. Review
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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

8 authors at 2 institutions in 1 country.

L L ShearsDepartment of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.
N Kawaharada
E Tzeng
T R Billiar
S C Watkins
I Kovesdi
A Lizonova
S M Pham
GenVec · USUniversity of Pittsburgh · US

Funding

NITRIC OXIDE AND HEPATIC FUNCTION IN SEPSIS AND TRAUMAR01GM044100 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BILLIAR, TIMOTHY R · 1995 to 2017
$1.9M
BLOCKING INTIMAL HYPERPLASIA FOLLOWING VASCULAR TRAUMAR29HL057854 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI TZENG, EDITH · 1997 to 2000
$105k
EFFECTORS IN THE ALLOGRAFT RESPONSER37AI016869 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SIMMONS, RICHARD L. · 1990 to 1999
–
NHLBI NIH HHS R29-HL-57854NIAID NIH HHS R37-AI-16869NIGMS NIH HHS R01-GM-44100
6 · The paper itself

Abstract

In cardiac transplantation, chronic rejection takes the form of an occlusive vasculopathy. The mechanism underlying this disorder remains unclear. The purpose of this study was to investigate the role nitric oxide (NO) may play in the development of allograft arteriosclerosis. Rat aortic allografts from ACI donors to Wistar Furth recipients with a strong genetic disparity in both major and minor histocompatibility antigens were used for transplantation. Allografts collected at 28 d were found to have significant increases in both inducible NO synthase (iNOS) mRNA and protein as well as in intimal thickness when compared with isografts. Inhibiting NO production with an iNOS inhibitor increased the intimal thickening by 57.2%, indicating that NO suppresses the development of allograft arteriosclerosis. Next, we evaluated the effect of cyclosporine (CsA) on iNOS expression and allograft arteriosclerosis. CsA (10 mg/kg/d) suppressed the expression of iNOS in response to balloon-induced aortic injury. Similarly, CsA inhibited iNOS expression in the aortic allografts, associated with a 65% increase in intimal thickening. Finally, we investigated the effect of adenoviral-mediated iNOS gene transfer on allograft arteriosclerosis. Transduction with iNOS using an adenoviral vector suppressed completely the development of allograft arteriosclerosis in both untreated recipients and recipients treated with CsA. These results suggest that the early immune-mediated upregulation in iNOS expression partially protects aortic allografts from the development of allograft arteriosclerosis, and that iNOS gene transfer strategies may prove useful in preventing the development of this otherwise untreatable disease process.

Indexed as

AnimalsAortaArteriosclerosisCyclosporineGenetic TherapyGraft RejectionHistocompatibility AntigensHyperplasiaImmunosuppressive AgentsNitric OxideNitric Oxide SynthaseOrgan TransplantationRatsRats, WistarTransplantation, HomologousTunica IntimaCyclosporineHistocompatibility AntigensImmunosuppressive AgentsNitric OxideNitric Oxide Synthase

Identifiers

PMID9329968
PMCPMC508394
OpenAlexW2085663049

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.