Evidence map›Paper›PMID 28821783›Full record

ArticleScientific reports2017

The NADPH oxidase NOX2 mediates loss of parvalbumin interneurons in traumatic brain injury: human autoptic immunohistochemical evidence.

Stefania Schiavone, Margherita Neri, Luigia Trabace, Emanuela Turillazzi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 53 citations in OpenAlex.

  1. Heart Rate Variability and Sympathetic Activity Is Modulated by Very Low-Calorie Ketogenic Diet.International journal of environmental research and public health · 2022
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  10. Treatment with the vascular endothelial growth factor-A antibody, bevacizumab, has sex-specific effects in a rat model of mild traumatic brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
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  20. Crosstalk between neuroinflammation and oxidative stress in epilepsy.Frontiers in cell and developmental biology · 2022
    Review
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

4 authors at 1 institution in 1 country.

Stefania SchiavoneDepartment of Clinical and Experimental Medicine, University of Foggia, Via Napoli 20, 71122, Foggia, Italy.
Margherita NeriDepartment of Clinical and Experimental Medicine, University of Foggia, Via Napoli 20, 71122, Foggia, Italy.ORCID 0000-0002-6459-1669
Luigia TrabaceDepartment of Clinical and Experimental Medicine, University of Foggia, Via Napoli 20, 71122, Foggia, Italy. luigia.trabace@unifg.it.
Emanuela TurillazziDepartment of Clinical and Experimental Medicine, University of Foggia, Via Napoli 20, 71122, Foggia, Italy.
University of Foggia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pharmacological interventions for traumatic brain injury (TBI) are limited. Together with parvalbumin (PV) loss, increased production of reactive oxygen species (ROS) by the NADPH oxidase NOX enzymes represents a key step in TBI. Here, we investigated the contribution of NOX2-derived oxidative stress to the loss of PV immunoreactivity associated to TBI, performing immunohistochemistry for NOX2, 8-hydroxy-2'-deoxyguanosine (8OHdG) and PV on post mortem brain samples of subjects died following TBI, subjects died from spontaneous intracerebral hemorrhage (SICH) and controls (CTRL). We detected an increased NOX2 expression and 8OHdG immunoreactivity in subjects died from TBI with respect to CTRL and SICH. NOX2 increase was mainly observed in GABAergic PV-positive interneurons, with a minor presence in microglia. No significant differences in other NADPH oxidase isoforms (NOX1 and NOX4) were detected among experimental groups. NOX2-derived oxidative stress elevation appeared a specific TBI-induced phenomenon, as no alterations in the nitrosative pathway were detected. Our results suggest that NOX2-derived oxidative stress might play a crucial role in the TBI-induced loss of PV-positive interneurons.

Indexed as

8-Hydroxy-2'-DeoxyguanosineAnimalsBrainBrain Injuries, TraumaticCell CountDeoxyguanosineHumansImmunohistochemistryInterneuronsMaleNADPH Oxidase 2Oxidation-ReductionOxidative StressParvalbuminsReactive Nitrogen SpeciesReactive Oxygen Species8-Hydroxy-2'-DeoxyguanosineDeoxyguanosineNADPH Oxidase 2ParvalbuminsReactive Nitrogen SpeciesReactive Oxygen Species

Identifiers

PMID28821783
PMCPMC5562735
OpenAlexW2747115532

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.