Evidence map›Paper›PMID 35716036›Full record

ArticleCell proliferation2022

Sprouty1 exerts a preventive effect on the initiation of psoriasis by inhibiting innate immune antimicrobial peptide cathelicidin and immunocytes.

Yuan Zhou, Ping Wang, Xue-Yan Chen, Bing-Xi Yan, Lilla Landeck, Zhao-Yuan Wang, Fan Xu, Min Zheng, Xiao-Yong Man

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

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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

9 authors at 2 institutions in 2 countries.

Yuan ZhouDepartment of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID https://orcid.org/0000-0002-2065-1922
Ping WangDepartment of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Xue-Yan ChenDepartment of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Bing-Xi YanDepartment of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Lilla LandeckDepartment of Dermatology, Ernst von Bergmann General Hospital, Potsdam, Germany.
Zhao-Yuan WangDepartment of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Fan XuDepartment of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Min ZhengDepartment of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Xiao-Yong ManDepartment of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID https://orcid.org/0000-0003-3331-5538
Second Affiliated Hospital of Zhejiang University · CNKlinikum Ernst von Bergmann · DE

Funding

National Natural Science Foundation of China 81630082National Natural Science Foundation of China 81773318National Natural Science Foundation of China 81930089National Natural Science Foundation of China 82103709
6 · The paper itself

Abstract

objectivesPsoriasis is an immune-mediated skin disease dominated by the cutaneous immune system. Keratinocytes have been considered important triggers that initiate psoriasis. The key molecules and events of keratinocytes that link the innate immune system in psoriasis must be investigated in more detail. Human psoriasis skin and primary human keratinocyte were detected in vitro. Epidermis specific transgenic mouse strain (Krt14-Sprouty1 tg) was used to further investigate psoriasis-like skin inflammation in vivo. MATERIALS AND

methodsBulk RNA sequencing of primary human keratinocyte screened differentially expressed genes, which was confirmed by quantitative real time PCR and Western Blot (WB). Moreover, we concomitantly reviewed open-accessed published RNAseq datasets of human psoriatic skin from GEO database. Immunohistochemical staining and immunofluorescence were used to detect Sprouty1 (SPRY1) expression in human psoriatic skin with and without anti-psoriasis treatments. Krt14-Sprouty1 tg was used to further investigate psoriasis-like skin inflammation, and followed by Hematoxylin and Eosin (HE) Staining, enzyme linked immunosorbent assay (ELISA), Western Blot and flow cytometry.

resultsOur data showed that Sprouty1 was decreased in psoriatic skin and keratinocytes. In imiquimod-induced psoriasis-like skin inflammation, the production of cathelicidin (camp/LL37) was inhibited by suppressing signal transducer and activator of transcription3 (Stat3) activation when Sprouty1 overexpressed in mouse epidermal keratinocytes. Moreover, CD11b+CCR2+ dendritic cells, IL-17A+ γδT cells, and Ly6C+ CD11c+ monocyte-derived dendritic cells were decreased in Krt14-Sprouty1 tg (STG) imiquimod-induced cutaneous inflammation.

conclusionsThese findings indicate that Sprouty1 expressed in keratinocytes has a suppressive role in imiquimod-induced skin inflammation mediated by inhibiting the production of cathelicidin. Collectively, Sprouty1 plays a preventive role in psoriatic skin. Our data provide new evidence for the pathogenesis of psoriatic keratinocytes, and the link cutaneous innate immunity, that indicated Sprouty1 is a potential novel therapeutic target.

Indexed as

Interleukin-17Membrane ProteinsPhosphoproteinsPsoriasisAnimalsAntimicrobial Cationic PeptidesAntimicrobial PeptidesCathelicidinsDisease Models, AnimalEosine Yellowish-(YS)HematoxylinHumansImiquimodImmunity, InnateInflammationKeratinocytesAntimicrobial Cationic PeptidesAntimicrobial PeptidesCathelicidinsEosine Yellowish-(YS)HematoxylinImiquimodInterleukin-17Membrane ProteinsPhosphoproteinsSPRY1 protein, human

Identifiers

PMID35716036
PMCPMC9528767
OpenAlexW4283073378

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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.