Evidence map›Paper›PMID 28272440›Full record

ArticleScientific reports2017

Epidermal CD147 expression plays a key role in IL-22-induced psoriatic dermatitis.

Cong Peng, ShengXi Zhang, Li Lei, Xu Zhang, Xuekun Jia, Zhongling Luo, Xiaoyan Huang, Yanhong Kuang, Weiqi Zeng, Juan Su and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. CD147/Basigin: From Integrative Molecular Hub to Translational Therapeutic Target.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  4. Review
  5. Signaling pathways and targeted therapies for psoriasis.Signal transduction and targeted therapy · 2023
    Review
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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

11 authors at 2 institutions in 1 country.

Cong PengDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
ShengXi ZhangDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Li LeiDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xu ZhangDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xuekun JiaDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Zhongling LuoDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xiaoyan HuangDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Yanhong KuangDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Weiqi ZengDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Juan SuDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xiang ChenDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Central South University · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is a chronic inflammatory skin disease characterized by abnormal keratinocyte proliferation and terminal differentiation. Interleukin-22 (IL-22) and the transcription factor Stat3 play pivotal roles in the pathogenesis of psoriasis. CD147 is a transmembrane glycosylation protein that belongs to the immunoglobulin superfamily. Our previous studies have shown that CD147 is a marker of high keratinocyte proliferation and poor keratinocyte differentiation as well as a psoriasis susceptibility gene. The current study demonstrates that CD147 is highly expressed in psoriatic skin lesions. Specific CD147 over-expression in the epidermis of K5-promoter transgenic mice promotes imiquimod (IMQ)-induced psoriasis-like inflammation characterized by acanthosis, granular layer loss and inflammatory cell infiltration. We also found that IL-22 increases CD147 transcription in vitro and in vivo and that Stat3 binds directly to the CD147 promoter between positions -854 and -440, suggesting that CD147 expression is up-regulated in patients with psoriasis through Stat3 activation. In addition, CD147 knockdown dramatically blocks IL-22-mediated Stat3 activation as well as IL-22-induced cytokine, chemokine and antimicrobial factor expression. Together, these findings show that CD147 is a novel and key mediator of IL-22-induced psoriatic alterations in the epidermis and might be a therapeutic target in patients with psoriasis.

Indexed as

AnimalsBasiginEpidermisHEK293 CellsHumansInterleukin-22InterleukinsKeratinocytesMiceMice, TransgenicPsoriasisBasiginBSG protein, humanInterleukin-22Interleukins

Identifiers

PMID28272440
PMCPMC5341158
OpenAlexW2592281904

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.