Evidence map›Paper›PMID 30733851›Full record

ArticleOxidative medicine and cellular longevity2019

Cold Physical Plasma Modulates p53 and Mitogen-Activated Protein Kinase Signaling in Keratinocytes.

Anke Schmidt, Sander Bekeschus, Katja Jarick, Sybille Hasse, Thomas von Woedtke, Kristian Wende

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
  2. Article
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  4. Wound healing and signaling pathways.Open life sciences · 2025
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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

6 authors at 2 institutions in 1 country.

Anke SchmidtLeibniz-Institute for Plasma Science and Technology e. V., Felix-Hausdorff-Str. 2, 17489 Greifswald, Germany.
Sander BekeschusLeibniz-Institute for Plasma Science and Technology e. V., Felix-Hausdorff-Str. 2, 17489 Greifswald, Germany.ORCID 0000-0002-8773-8862
Katja JarickLeibniz-Institute for Plasma Science and Technology e. V., Felix-Hausdorff-Str. 2, 17489 Greifswald, Germany.
Sybille HasseLeibniz-Institute for Plasma Science and Technology e. V., Felix-Hausdorff-Str. 2, 17489 Greifswald, Germany.
Thomas von WoedtkeLeibniz-Institute for Plasma Science and Technology e. V., Felix-Hausdorff-Str. 2, 17489 Greifswald, Germany.
Kristian WendeLeibniz-Institute for Plasma Science and Technology e. V., Felix-Hausdorff-Str. 2, 17489 Greifswald, Germany.ORCID 0000-0001-5217-0683
Leibniz Institute for Plasma Science and Technology · DEUniversitätsmedizin Greifswald · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small reactive oxygen and nitrogen species (ROS/RNS) driven signaling plays a significant role in wound healing processes by controlling cell functionality and wound phase transitions. The application of cold atmospheric pressure plasma (CAP), a partially ionized gas expelling a variety of ROS and RNS, was shown to be effective in chronic wound management and contrastingly also in malignant diseases. The underlying molecular mechanisms are not well understood but redox signaling events are involved. As a central player, the cellular tumor antigen p53 governs regulatory networks controlling proliferation, death, or metabolism, all of which are grossly modulated by anti- and prooxidant signals. Using a human skin cell model, a transient phosphorylation and nuclear translocation of p53, preceded by the phosphorylation of upstream serine- (ATM) and serine/threonine-protein kinase (ATR), was detected after CAP treatment. Results indicate that ATM acts as a direct redox sensor without relevant contribution of phosphorylation of the histone A2X, a marker of DNA damage. Downstream events are the activation of checkpoint kinases Chk1/2 and several mitogen-activated (MAP) kinases. Subsequently, the expression of MAP kinase signaling effectors (e.g., heat shock protein Hsp27), epithelium derived growth factors, and cytokines (Interleukins 6 + 8) was increased. A number of p53 downstream effectors pointed at a decrease of cell growth due to DNA repair processes. In summary, CAP treatment led to an activation of cell repair and defense mechanisms including a modulation of paracrine inflammatory signals emphasizing the role of prooxidant species in CAP-related cell signaling.

Indexed as

HumansKeratinocytesMitogen-Activated Protein KinasesPlasma GasesSignal TransductionTumor Suppressor Protein p53Mitogen-Activated Protein KinasesPlasma GasesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID30733851
PMCPMC6348845
OpenAlexW2909655997

What OpenQuestion holds

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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.