Evidence map›Paper›PMID 30194425›Full record

ArticleScientific reports2018

Low-dose calcipotriol can elicit wound closure, anti-microbial, and anti-neoplastic effects in epidermolysis bullosa keratinocytes.

Christina Guttmann-Gruber, Birgit Tockner, Cornelia Scharler, Clemens Hüttner, John E Common, Angeline S L Tay, Simon L I J Denil, Alfred Klausegger, Andrea Trost, Jenny Breitenbach and 10 more

Abstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Trial
  2. Trial
  3. Article
  4. Review
  5. Article
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  8. Topical Calcipotriol Plus Imiquimod Immunotherapy for Nonkeratinocyte Skin Cancers.JID innovations : skin science from molecules to population health · 2023
    Article
  9. Article
  10. Review
  11. Article
  12. Keratins as an Inflammation Trigger Point in Epidermolysis Bullosa Simplex.International journal of molecular sciences · 2021
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
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

20 authors.

Christina Guttmann-GruberEB House Austria, Research Program for Molecular Therapy of Genodermatoses, Department of Dermatology, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria. c.gruber@salk.at.
Birgit TocknerEB House Austria, Research Program for Molecular Therapy of Genodermatoses, Department of Dermatology, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria.
Cornelia ScharlerExperimental & Clinical Cell Therapy Institute, Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), PMU Salzburg, Salzburg, Austria.
Clemens HüttnerEB House Austria, Research Program for Molecular Therapy of Genodermatoses, Department of Dermatology, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria.
John E CommonInstitute of Medical Biology, A*STAR, 8A Biomedical Grove, Immunos #06-08, Singapore, Singapore.ORCID 0000-0002-3280-7365
Angeline S L TayInstitute of Medical Biology, A*STAR, 8A Biomedical Grove, Immunos #06-08, Singapore, Singapore.
Simon L I J DenilInstitute of Medical Biology, A*STAR, 8A Biomedical Grove, Immunos #06-08, Singapore, Singapore.
Alfred KlauseggerEB House Austria, Research Program for Molecular Therapy of Genodermatoses, Department of Dermatology, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria.
Andrea TrostUniversity Clinic of Ophthalmology and Optometry, Research Program for Ophthalmology and Glaucoma Research, Paracelsus Medical University Salzburg, Salzburg, Austria.
Jenny BreitenbachEB House Austria, Research Program for Molecular Therapy of Genodermatoses, Department of Dermatology, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria.
Peter SchnitzhoferEB House Austria, Research Program for Molecular Therapy of Genodermatoses, Department of Dermatology, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria.
Peter HofbauerLandesapotheke Salzburg, Department of Production, Hospital Pharmacy, Salzburg, Austria.
Martin WolkersdorferLandesapotheke Salzburg, Department of Production, Hospital Pharmacy, Salzburg, Austria.
Anja DiemEB House Austria, Research Program for Molecular Therapy of Genodermatoses, Department of Dermatology, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria.
Martin LaimerDepartment of Dermatology, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria.
Dirk StrunkExperimental & Clinical Cell Therapy Institute, Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), PMU Salzburg, Salzburg, Austria.ORCID 0000-0003-1810-867X
Johann W BauerDepartment of Dermatology, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria.
Julia ReicheltEB House Austria, Research Program for Molecular Therapy of Genodermatoses, Department of Dermatology, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria.ORCID 0000-0002-4358-7011
Roland LangDepartment of Dermatology, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria.
Josefina Piñón HofbauerEB House Austria, Research Program for Molecular Therapy of Genodermatoses, Department of Dermatology, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recessive dystrophic epidermolysis bullosa (RDEB) patients suffer from chronic and repeatedly infected wounds predisposing them to the development of aggressive and life-threatening skin cancer in these areas. Vitamin D3 is an often neglected but critical factor for wound healing. Intact skin possesses the entire enzymatic machinery required to produce active 1-alpha,25-dihydroxyvitamin D3 (calcitriol), underscoring its significance to proper skin function. Injury enhances calcitriol production, inducing the expression of calcitriol target genes including the antimicrobial peptide cathelicidin (hCAP18), an essential component of the innate immune system and an important wound healing factor. We found significantly reduced hCAP18 expression in a subset of RDEB keratinocytes which could be restored by calcipotriol treatment. Reduced scratch closure in RDEB cell monolayers was enhanced up to 2-fold by calcipotriol treatment, and the secretome of calcipotriol-treated cells additionally showed increased antimicrobial activity. Calcipotriol exhibited anti-neoplastic effects, suppressing the clonogenicity and proliferation of RDEB tumor cells. The combined wound healing, anti-microbial, and anti-neoplastic effects indicate that calcipotriol may represent a vital therapeutic option for RDEB patients which we could demonstrate in a single-patient observation study.

Indexed as

Wound HealingAgedAnti-Bacterial AgentsAntimicrobial Cationic PeptidesAntineoplastic AgentsCalcitriolCathelicidinsCell LineCells, CulturedDermatologic AgentsEpidermolysis BullosaHumansKeratinocytesMaleAnti-Bacterial AgentsAntimicrobial Cationic PeptidesAntineoplastic AgentscalcipotrieneCalcitriolCathelicidinsDermatologic Agents

Identifiers

PMID30194425
PMCPMC6128832

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.