Evidence map›Paper›PMID 27624276›Full record

ArticleScientific reports2016

Redox/methylation mediated abnormal DNA methylation as regulators of ambient fine particulate matter-induced neurodevelopment related impairment in human neuronal cells.

Hongying Wei, Fan Liang, Ge Meng, Zhiqing Nie, Ren Zhou, Wei Cheng, Xiaomeng Wu, Yan Feng, Yan Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 72 citations in OpenAlex.

  1. Trial
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  9. Exosome-encapsulated lncRNA HOTAIRM1 contributes to PMScience China. Life sciences · 2024
    Article
  10. Differential DNA methylation in the brain as potential mediator of the association between traffic-related PMAlzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Toxicological Effects of Fine Particulate Matter (PMWater, air, and soil pollution · 2023
    Review
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  19. Article
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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

9 authors at 3 institutions in 1 country.

Hongying WeiShanghai Jiao Tong University School of Public Health; Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Shanghai 200025, China.
Fan LiangShanghai Jiao Tong University School of Public Health; Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Shanghai 200025, China.
Ge MengShanghai Jiao Tong University School of Public Health; Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Shanghai 200025, China.
Zhiqing NieShanghai Jiao Tong University School of Environmental Science and Engineering, Shanghai, 200240, China.
Ren ZhouShanghai Jiao Tong University School of Public Health; Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Shanghai 200025, China.
Wei ChengShanghai Jiao Tong University School of Public Health; Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Shanghai 200025, China.
Xiaomeng WuShanghai Jiao Tong University School of Public Health; Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Shanghai 200025, China.
Yan FengShanghai Jiao Tong University School of Public Health; Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Shanghai 200025, China.
Yan WangShanghai Jiao Tong University School of Public Health; Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Shanghai 200025, China.
Shanghai Jiao Tong University · CNShanghai Ninth People's Hospital · CNTongren Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fine particulate matter (PM2.5) has been implicated as a risk factor for neurodevelopmental disorders including autism in children. However, the underlying biological mechanism remains unclear. DNA methylation is suggested to be a fundamental mechanism for the neuronal responses to environmental cues. We prepared whole particle of PM2.5 (PM2.5), water-soluble extracts (Pw), organic extracts (Po) and carbon core component (Pc) and characterized their chemical constitutes. We found that PM2.5 induced significant redox imbalance, decreased the levels of intercellular methyl donor S-adenosylmethionine and caused global DNA hypomethylation. Furthermore, PM2.5 exposure triggered gene-specific promoter DNA hypo- or hypermethylation and abnormal mRNA expression of autism candidate genes. PM2.5-induced DNA hypermethylation in promoter regions of synapse related genes were associated with the decreases in their mRNA and protein expression. The inhibiting effects of antioxidative reagents, a methylation-supporting agent and a DNA methyltransferase inhibitor demonstrated the involvement of redox/methylation mechanism in PM2.5-induced abnormal DNA methylation patterns and synaptic protein expression. The biological effects above generally followed a sequence of PM2.5 ≥ Pwo > Po > Pw > Pc. Our results implicated a novel epigenetic mechanism for the neurodevelopmental toxicity of particulate air pollution, and that eliminating the chemical components could mitigate the neurotoxicity of PM2.5.

Indexed as

DNA MethylationAntioxidantsAutistic DisorderCell Line, TumorGenetic Association StudiesHumansNervous SystemNeuronsOxidation-ReductionOxidative StressParticulate MatterPromoter Regions, GeneticRNA, MessengerSynapsesUp-RegulationAntioxidantsParticulate MatterRNA, Messenger

Identifiers

PMID27624276
PMCPMC5022064
OpenAlexW2518947353

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.