Evidence map›Paper›PMID 25431847›Full record

ArticleThe Journal of investigative dermatology2015

Electrical stimulation enhances epidermal proliferation in human cutaneous wounds by modulating p53-SIVA1 interaction.

Anil Sebastian, Syed A Iqbal, James Colthurst, Susan W Volk, Ardeshir Bayat

Abstract read
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In one paragraph

Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 62 citations in OpenAlex.

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  10. Electrical Stimulation to Enhance Wound Healing.Journal of functional biomaterials · 2021
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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

5 authors at 3 institutions in 2 countries.

Anil SebastianPlastic and Reconstructive Surgery Research, Institute of Inflammation and Repair, Manchester Institute of Biotechnology, School of Medical and Human Sciences, University of Manchester, Manchester, UK.
Syed A IqbalPlastic and Reconstructive Surgery Research, Institute of Inflammation and Repair, Manchester Institute of Biotechnology, School of Medical and Human Sciences, University of Manchester, Manchester, UK.
James ColthurstFenzian Ltd, Hungerford, Berkshire, UK.
Susan W VolkSection of Surgery, Department of Clinical Studies, University of Pennsylvania School of Veterinary Medicine, Philadelphia, Pennsylvania, USA.
Ardeshir BayatPlastic and Reconstructive Surgery Research, Institute of Inflammation and Repair, Manchester Institute of Biotechnology, School of Medical and Human Sciences, University of Manchester, Manchester, UK; Centre for Dermatology, Institute of Inflammation and Repair, University of Manchester, Manchester, UK; Manchester Academic Health Science Centre, South Manchester University Hospital Foundation Trust, Wythenshawe Hospital, Manchester, UK. Electronic address: ardeshir.bayat@manchester.ac.uk.
University of Manchester · GBManchester Academic Health Science Centre · GBUniversity of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cutaneous wounds establish endogenous "wound current" upon injury until re-epithelialization is complete. Keratinocyte proliferation, regulated partly by p53, is required for epidermal closure. SIVA1 promotes human double minute 2 homolog (HDM2)-mediated p53 regulation. However, the role of SIVA1 in wound healing is obscure. Here, we report that electrical stimulation (ES) accelerates wound healing by upregulating SIVA1 and its subsequent ability to modulate p53 activities. Cultured donut-shaped human skin explants, subjected to ES, exhibited better epidermal stratification, increased proliferation, and upregulation of gene and protein expression of HDM2/SIVA1, compared with non-ES-treated explants. ES significantly increased in vitro keratinocyte proliferation and phospho-p53-SIVA1 interaction; however, this showed stable expression of phospho-p53, which increased significantly in the absence of SIVA1. Here, HDM2 alone was unable to downregulate nuclear-accumulated phospho-p53, which was evident from decreased proliferation and increased sub-G1 population seen by flow cytometry. Further examination of the epidermis of human cutaneous wounds showed higher p53-SIVA1 coexpression and proliferation 7 days after injury in ES-treated wounds compared with control wounds. In summary, ES-inducible SIVA1 modulates p53 activities in proliferating keratinocytes, and exogenous ES affects p53/HDM2/SIVA1 axis leading to increased proliferation during re-epithelialization. This highlights ES as a potential strategy for enhancing cutaneous repair.

Indexed as

Electric StimulationApoptosis Regulatory ProteinsCell CycleCell DivisionCell ProliferationEpidermisFlow CytometryG1 PhaseGene Expression RegulationHumansImmunohistochemistryKeratinocytesOrgan Culture TechniquesProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-mdm2SkinApoptosis Regulatory ProteinsMDM2 protein, humanProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-mdm2SIVA1 protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID25431847
OpenAlexW2004668907

What OpenQuestion holds

Textmetadata
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.