Evidence map›Paper›PMID 32863235›Full record

ArticleRedox biology2020

Non-thermal dielectric-barrier discharge plasma induces reactive oxygen species by epigenetically modifying the expression of NADPH oxidase family genes in keratinocytes.

Kyoung Ah Kang, Mei Jing Piao, Sangheum Eom, Sung-Young Yoon, Seungmin Ryu, Seong Bong Kim, Joo Mi Yi, Jin Won Hyun

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2020. 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
1.1field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Effects of non-thermal atmospheric plasma on protein.Journal of clinical biochemistry and nutrition · 2022
    Article
  9. Article
  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

8 authors at 4 institutions in 1 country.

Kyoung Ah KangDepartment of Biochemistry, College of Medicine, Jeju National University, Jeju, 63243, Republic of Korea.
Mei Jing PiaoDepartment of Biochemistry, College of Medicine, Jeju National University, Jeju, 63243, Republic of Korea.
Sangheum EomPlasma Technology Research Center of National Fusion Research Institute, Gunsan, 54004, Republic of Korea.
Sung-Young YoonPlasma Technology Research Center of National Fusion Research Institute, Gunsan, 54004, Republic of Korea.
Seungmin RyuPlasma Technology Research Center of National Fusion Research Institute, Gunsan, 54004, Republic of Korea.
Seong Bong KimPlasma Technology Research Center of National Fusion Research Institute, Gunsan, 54004, Republic of Korea.
Joo Mi YiDepartment of Microbiology and Immunology, Inje University College of Medicine, Busan, 47392, Republic of Korea.
Jin Won HyunDepartment of Biochemistry, College of Medicine, Jeju National University, Jeju, 63243, Republic of Korea. Electronic address: jinwonh@jejunu.ac.kr.
Korea Institute of Fusion Energy · KRJeju National University · KRInje University · KRJeju National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have previously shown that non-thermal dielectric-barrier discharge (DBD) plasma induces the generation of reactive oxygen species (ROS) in cells; however, the underlying mechanism has not been elucidated. This study aimed to identify the mechanisms through which DBD plasma induces the expression of NADPH oxidase (NOX) family members by epigenetic modification in human keratinocytes (HaCaT). Cell exposure to DBD plasma in 10% oxygen and 90% argon resulted in the generation of ROS, triggering oxidative stress that manifested in various forms, including lipid membrane peroxidation, DNA base modification, and protein carbonylation. DBD plasma upregulated the expression of NOX1, NOX5, and DUOX2 at the mRNA and protein levels; and siRNAs targeting NOX1, NOX5, and DUOX2 attenuated the generation of DBD plasma-induced ROS. DBD plasma upregulated the transcriptional activators TET1, MLL1, and HAT1 and downregulated the transcriptional repressors DNMT1, EZH2, and HDAC1. Additionally, DBD plasma increased the binding of transcriptional activators and decreased the binding of transcriptional repressors to the DUOX2 promoter. Methyl-specific polymerase chain reaction and bisulfite sequencing indicated that DBD plasma decreased methylation at the DUOX2 promoter. These results suggest that DBD plasma induces ROS generation by enhancing the expression of the NOX system through epigenetic DNA and histone modifications.

Indexed as

KeratinocytesNADPH OxidasesHumansMixed Function OxygenasesNADPH Oxidase 1NADPH Oxidase 4NADPH Oxidase 5Oxidation-ReductionOxidative StressProto-Oncogene ProteinsReactive Oxygen SpeciesMixed Function OxygenasesNADPH Oxidase 1NADPH Oxidase 4NADPH Oxidase 5NADPH OxidasesProto-Oncogene ProteinsReactive Oxygen SpeciesTET1 protein, humanDielectric-barrier discharge plasmaDNA methylationHistone modificationNOX familyReactive oxygen species

Identifiers

PMID32863235
PMCPMC7472924
OpenAlexW3080839997

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.