Evidence map›Paper›PMID 28880721›Full record

ArticleInternational journal of radiation biology2017

Role of NADPH oxidase in radiation-induced pro-oxidative and pro-inflammatory pathways in mouse brain.

Hyung Joon Cho, Won Hee Lee, Olivia Min Ha Hwang, William E Sonntag, Yong Woo Lee

Abstract read
In one paragraph

Article in International journal of radiation biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Microglia as Therapeutic Target for Radiation-Induced Brain Injury.International journal of molecular sciences · 2022
    Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. 1α,25(OH)Frontiers in pharmacology · 2020
    Article
  7. Article
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  10. 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.

Hyung Joon Choa Department of Biochemistry and Molecular Biology , University of Miami Miller School of Medicine , Miami , FL , USA.ORCID 0000-0002-7481-6841
Won Hee Leeb Stanford Cardiovascular Institute , Stanford University , Stanford , CA , USA.ORCID 0000-0001-8534-9639
Olivia Min Ha Hwangc Department of Biomedical Engineering and Mechanics , Virginia Tech , Blacksburg , VA , USA.
William E Sonntagd Department of Geriatric Medicine , University of Oklahoma Health Sciences Center , Oklahoma City , OK , USA.
Yong Woo Leec Department of Biomedical Engineering and Mechanics , Virginia Tech , Blacksburg , VA , USA.ORCID 0000-0003-2363-0278

Funding

Effects of Radiation on Brain Microvasculature and CognitionR01NS056218 · NINDS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CSISZAR, ANNA, SONNTAG, WILLIAM EDMUND · 2007 to 2018
$3.6M
NINDS NIH HHS R01 NS056218
6 · The paper itself

Abstract

purposeThe present study was designed to investigate our hypothesis that NADPH oxidase plays a role in radiation-induced pro-oxidative and pro-inflammatory environments in the brain. MATERIALS AND

methodsC57BL/6 mice received either fractionated whole brain irradiation or sham-irradiation. The mRNA expression levels of pro-inflammatory mediators, such as TNF-α and MCP-1, were determined by quantitative real-time RT-PCR. The protein expression levels of TNF-α, MCP-1, NOX-2 and Iba1 were detected by immunofluorescence staining. The levels of ROS were visualized by in situ DHE fluorescence staining.

resultsA significant up-regulation of mRNA and protein expression levels of TNF-α and MCP-1 was observed in irradiated mouse brains. Additionally, immunofluorescence staining of Iba1 showed a marked increase of microglial activation in mouse brain after irradiation. Moreover, in situ DHE fluorescence staining revealed that fractionated whole brain irradiation significantly increased production of ROS. Furthermore, a significant increase in immunoreactivity of NOX-2 was detected in mouse brain after irradiation. On the contrary, an enhanced ROS generation in mouse brain after irradiation was markedly attenuated in the presence of NOX inhibitors or NOX-2 neutralizing antibody.

conclusionsThese results suggest that NOX-2 may play a role in fractionated whole brain irradiation-induced pro-oxidative and pro-inflammatory pathways in mouse brain.

Indexed as

AnimalsBrainChemokine CCL2Dose Fractionation, RadiationGene Expression Regulation, EnzymologicInflammationMaleMembrane GlycoproteinsMiceMice, Inbred C57BLMicrogliaNADPH Oxidase 2NADPH OxidasesOxidation-ReductionOxidative StressRNA, MessengerCcl2 protein, mouseChemokine CCL2Cybb protein, mouseMembrane GlycoproteinsNADPH Oxidase 2NADPH OxidasesRNA, MessengerTumor Necrosis Factor-alphaFractionated whole brain irradiationinflammationNOX-2ROS

Identifiers

PMID28880721
PMCPMC6080279

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Registered trials

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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.