Evidence map›Paper›PMID 15949035›Full record

ArticleBMC cancer2005

Overexpression of extracellular superoxide dismutase reduces acute radiation induced lung toxicity.

Zahid N Rabbani, Mitchell S Anscher, Rodney J Folz, Emerald Archer, Hong Huang, Liguang Chen, Maria L Golson, Thaddeus S Samulski, Mark W Dewhirst, Zeljko Vujaskovic

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.3field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 100 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

Zahid N RabbaniDepartment of Radiation Oncology, Duke University Medical Center, Durham, North Carolina, USA. zahid@radonc.duke.edu
Mitchell S Anscher
Rodney J Folz
Emerald Archer
Hong Huang
Liguang Chen
Maria L Golson
Thaddeus S Samulski
Mark W Dewhirst
Zeljko Vujaskovic
Duke Medical Center · USDuke University · USDuke University Hospital · US

Funding

Mechanism of hypoxia mediated radiation lung injuryR01CA098452 · NCI · DUKE UNIVERSITY · PI VUJASKOVIC, ZELJKO · 2003 to 2006
$1.1M
NCI NIH HHS CA98452NCI NIH HHS R01 CA098452
6 · The paper itself

Abstract

backgroundAcute RT-induced damage to the lung is characterized by inflammatory changes, which proceed to the development of fibrotic lesions in the late phase of injury. Ultimately, complete structural ablation will ensue, if the source of inflammatory/fibrogenic mediators and oxidative stress is not removed or attenuated. Therefore, the purpose of this study is to determine whether overexpression of extracellular superoxide dismutase (EC-SOD) in mice ameliorates acute radiation induced injury by inhibiting activation of TGFbeta1 and downregulating the Smad 3 arm of its signal transduction pathway.

methodsWhole thorax radiation (single dose, 15 Gy) was delivered to EC-SOD overexpressing transgenic (XRT-TG) and wild-type (XRT-WT) animals. Mice were sacrificed at 1 day, 1 week, 3, 6, 10 and 14 weeks. Breathing rates, right lung weights, total/differential leukocyte count, activated TGFbeta1 and components of its signal transduction pathway (Smad 3 and p-Smad 2/3) were assessed to determine lung injury.

resultsIrradiated wild-type (XRT-WT) animals exhibited time dependent increase in breathing rates and right lung weights, whereas these parameters were significantly less increased (p < 0.05) at 3, 6, 10 and 14 weeks in irradiated transgenic (XRT-TG) mice. An inflammatory response characterized predominantly by macrophage infiltration was pronounced in XRT-WT mice. This acute inflammation was significantly attenuated (p < 0.05) in XRT-TG animals at 1, 3, 6 and 14 weeks. Expression of activated TGFbeta1 and components of its signal transduction pathway were significantly reduced (p < 0.05) at later time-points in XRT-TG vs. XRT-WT.

conclusionThis study shows that overexpression of EC-SOD confers protection against RT-induced acute lung injury. EC-SOD appears to work, in part, via an attenuation of the macrophage response and also decreases TGFbeta1 activation with a subsequent downregulation of the profibrotic TGFbeta pathway.

Indexed as

Radiation InjuriesAnimalsBronchoalveolar Lavage FluidDown-RegulationExtracellular MatrixExtracellular SpaceHumansImmunohistochemistryInflammationLungMacrophagesMiceMice, Inbred C3HMice, Inbred C57BLMice, TransgenicOxidative StressSmad3 ProteinSuperoxide DismutaseTGFB1 protein, humanTgfb1 protein, mouseTransforming Growth Factor betaTransforming Growth Factor beta1

Identifiers

PMID15949035
PMCPMC1177930
OpenAlexW1901986041

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.