Evidence map›Paper›PMID 26474319›Full record

ArticlePloS one2015

IL-22/STAT3-Induced Increases in SLURP1 Expression within Psoriatic Lesions Exerts Antimicrobial Effects against Staphylococcus aureus.

Yasuhiro Moriwaki, Kiyoko Takada, Toshinori Nagasaki, Natsuki Kubo, Tomohiro Ishii, Kazuaki Kose, Taihei Kageyama, Shoutaro Tsuji, Koichiro Kawashima, Hidemi Misawa

RetractedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Molecular biology research communications · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
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  7. Infection-provoked psoriasis: Induced or aggravated (Review).Experimental and therapeutic medicine · 2021
    Review
  8. Clonal Vγ6Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  9. Effect of RNA Interference TargetingChinese medical journal · 2018
    Article
  10. Article
  11. Article
  12. Effects of RNA interference combined with ultrasonic irradiation and SonoVue microbubbles on expression of STAT3 gene in keratinocytes of psoriatic lesions.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2017
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Yasuhiro MoriwakiDepartment of Pharmacology, Faculty of Pharmacy, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Kiyoko TakadaDepartment of Pharmacology, Faculty of Pharmacy, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Toshinori NagasakiDepartment of Pharmacology, Faculty of Pharmacy, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Natsuki KuboDepartment of Pharmacology, Faculty of Pharmacy, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Tomohiro IshiiDepartment of Pharmacology, Faculty of Pharmacy, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Kazuaki KoseDepartment of Pharmacology, Faculty of Pharmacy, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Taihei KageyamaMolecular Diagnostics Project, Kanagawa Cancer Center Research Institute, Yokohama, Kanagawa, Japan.
Shoutaro TsujiMolecular Diagnostics Project, Kanagawa Cancer Center Research Institute, Yokohama, Kanagawa, Japan.
Koichiro KawashimaDepartment of Molecular Pharmacology, Kitasato University School of Pharmacy, Minato-ku, Tokyo, Japan.
Hidemi MisawaDepartment of Pharmacology, Faculty of Pharmacy, Keio University, Minato-ku, Tokyo 105-8512, Japan.
Keio University · JPKanagawa Cancer CenterKitasato University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSLURP1 is the causal gene for Mal de Meleda (MDM), an autosomal recessive skin disorder characterized by diffuse palmoplantar keratoderma and transgressive keratosis. Moreover, although SLURP1 likely serves as an important proliferation/differentiation factor in keratinocytes, the possible relation between SLURP1 and other skin diseases, such as psoriasis and atopic dermatitis, has not been studied, and the pathophysiological control of SLURP1 expression in keratinocytes is largely unknown.

objectivesOur aim was to examine the involvement of SLURP1 in the pathophysiology of psoriasis using an imiquimod (IMQ)-induced psoriasis model mice and normal human epidermal keratinocytes (NHEKs).

resultsSLURP1 expression was up-regulated in the skin of IMQ-induced psoriasis model mice. In NHEKs stimulated with the inflammatory cytokines IL-17, IL-22 and TNF-α, which are reportedly expressed in psoriatic lesions, SLURP1 mRNA expression was significantly up-regulated by IL-22 but not the other two cytokines. The stimulatory effect of IL-22 was completely suppressed in NHEKs treated with a STAT3 inhibitor or transfected with siRNA targeting STAT3. Because IL-22 induces production of antimicrobial proteins in epithelial cells, the antibacterial activity of SLURP1 was assessed against Staphylococcus aureus (S. aureus), which is known to be associated with disease severity in psoriasis. SLURP1 significantly suppressed the growth of S. aureus.

conclusionsThese results indicate SLURP1 participates in pathophysiology of psoriasis by regulating keratinocyte proliferation and differentiation, and by suppressing the growth of S. aureus.

Indexed as

AminoquinolinesAnimalsAntigens, LyFemaleHomeostasisHumansImiquimodInterleukin-22InterleukinsKeratinocytesMiceMice, Inbred BALB CPsoriasisSkinStaphylococcus aureusSTAT3 Transcription FactorAminoquinolinesAntigens, LyImiquimodInterleukin-22InterleukinsSLURP1 protein, humanSLURP-1 protein, mouseSTAT3 Transcription FactorUrokinase-Type Plasminogen Activator

Identifiers

PMID26474319
PMCPMC4608685
OpenAlexW2192345019

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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.