Evidence map›Paper›PMID 29872728›Full record

ArticleBiochemistry and biophysics reports2018

Involvement of NADPH oxidase 1 in UVB-induced cell signaling and cytotoxicity in human keratinocytes.

Azela Glady, Manami Tanaka, Catharina Sagita Moniaga, Masato Yasui, Mariko Hara-Chikuma

Open access · goldAbstract read
In one paragraph

Article in Biochemistry and biophysics reports, 2018. 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
2.7field-weighted citation impact, top 10% 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, 51 citations in OpenAlex.

  1. Article
  2. Review
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  15. Gut Bacteria ofACS omega · 2021
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  17. Diversified Stimuli-Induced Inflammatory Pathways Cause Skin Pigmentation.International journal of molecular sciences · 2021
    Review
  18. Protective Effect of Anthocyanin-Enriched Polyphenols fromAntioxidants (Basel, Switzerland) · 2021
    Article
  19. Article
  20. Topical Administration of 15-Deoxy-Mediators of inflammation · 2021
    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 at 1 institution in 1 country.

Azela GladyDepartment of Pharmacology, Keio University School of Medicine, 35 Shinano-machi, Shinjuku-ku, Tokyo 160-8582, Japan.
Manami TanakaDepartment of Pharmacology, Keio University School of Medicine, 35 Shinano-machi, Shinjuku-ku, Tokyo 160-8582, Japan.
Catharina Sagita MoniagaDepartment of Pharmacology, Keio University School of Medicine, 35 Shinano-machi, Shinjuku-ku, Tokyo 160-8582, Japan.
Masato YasuiDepartment of Pharmacology, Keio University School of Medicine, 35 Shinano-machi, Shinjuku-ku, Tokyo 160-8582, Japan.
Mariko Hara-ChikumaDepartment of Pharmacology, Keio University School of Medicine, 35 Shinano-machi, Shinjuku-ku, Tokyo 160-8582, Japan.
Keio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Members of NADPH oxidase (Nox) enzyme family are important sources of reactive oxygen species (ROS) and are known to be involved in several physiological functions in response to various stimuli including UV irradiation. UVB-induced ROS have been associated with inflammation, cytotoxicity, cell death, or DNA damage in human keratinocytes. However, the source and the role of UVB-induced ROS remain undefined. Here, we show that Nox1 is involved in UVB-induced p38/MAPK activation and cytotoxicity via ROS generation in keratinocytes. Nox1 knockdown or inhibitor decreased UVB-induced ROS production in human keratinocytes. Nox1 knockdown impaired UVB-induced p38 activation, accompanied by reduced IL-6 levels and attenuated cell toxicity. Treatment of cells with N-acetyl-L-cysteine (NAC), a potent ROS scavenger, suppressed p38 activation as well as consequent IL-6 production and cytotoxicity in response to UVB exposure. p38 inhibitor also suppressed UVB-induced IL-6 production and cytotoxicity. Furthermore, the blockade of IL-6 production by IL-6 neutralizing antibody reduced UVB-induced cell toxicity.

Indexed as

ASK1, Apoptosis signal-regulating kinase 1Bax, BCL2-associated X proteinCytotoxicityDNA, Deoxyribonucleic acidDPI, DiphenyleneiodoniumErk, Extracellular Signal-regulated kinaseGM-CSF, Granulocyte-macrophage colony-stimulating factorH2DCFDA, Fluorescent 2',7'-dichlorofluorescein diacetateH2O2, Hydrogen peroxideIL-6, Interleukin-6JNK, Jun N-terminal kinases;KeratinocyteLDH, Lactate dehydrogenaseMAPK, Mitogen-activated protein kinaseMKK, MAP KinaseMKP, MAPK phosphataseNAC, N-acetyl cysteineNADPH oxidase 1NF-κB, Nuclear factor kappa B;NOX, NADPH oxidaseO2-, SuperoxideOH, Hydroxyl radicalP38/MAP kinasePBS, Phosphate-buffered salineReactive oxygen speciesRNA, Ribonucleic acidROS, Reactive Oxygen SpeciesSTAT3, Signal transducer and activator of transcription 3TNF-α, Tumor necrosis factor-alphaUVBUV, Ultraviolet

Identifiers

PMID29872728
PMCPMC5986629
OpenAlexW2794443462

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.