Evidence map›Paper›PMID 26269426›Full record

ArticleOpen biology2015

Analysis of epithelial-mesenchymal transition markers in psoriatic epidermal keratinocytes.

Xiao-Yong Man, Xi-Bei Chen, Wei Li, Lilla Landeck, Ting-Ting Dou, Jia-Qi Chen, Jiong Zhou, Sui-Qing Cai, Min Zheng

Open access · goldAbstract read
In one paragraph

Article in Open biology, 2015. 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
1.0field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  4. Article
  5. IQGAP3 Is an Important Mediator of Skin Inflammatory Diseases.International journal of molecular sciences · 2024
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  6. 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

9 authors at 2 institutions in 2 countries.

Xiao-Yong ManDepartment of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People's Republic of China manxy@zju.edu.cn.
Xi-Bei ChenDepartment of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People's Republic of China.
Wei LiDepartment of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People's Republic of China.
Lilla LandeckDepartment of Dermatology, Ernst von Bergmann General Hospital, Teaching Hospital of Charité-University, Potsdam, Germany.
Ting-Ting DouDepartment of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People's Republic of China.
Jia-Qi ChenDepartment of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People's Republic of China.
Jiong ZhouDepartment of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People's Republic of China.
Sui-Qing CaiDepartment of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People's Republic of China.
Min ZhengDepartment of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People's Republic of China minz@zju.edu.cn.
Second Affiliated Hospital of Zhejiang University · CNCharité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is similar to endpoints of epithelial-mesenchymal transition (EMT), a process of epithelial cells transformed into fibroblast-like cells. The molecular epithelial and mesenchymal markers were analysed in psoriatic keratinocytes. No obvious alteration of epithelial markers E-cadherin (E-cad), keratin 10 (K10), K14 and K16 was detected in psoriatic keratinocytes. However, significantly increased expression of Vim, FN, plasminogen activator inhibitor 1 (PAI-1) and Slug was seen. IL-17A and IL-13 at 50 ng ml(-1) strongly decreased expression of K10, Vim and FN. TGF-β1 at 50 ng ml(-1) promoted the production of N-cad, Vim, FN and PAI-1. Slug was decreased by dexamethasone (Dex), but E-cad was upregulated by Dex. Silencing of ERK partially increased E-cad and K16, but remarkably inhibited K14, FN, Vim, β-catenin, Slug and α5 integrin. Moreover, inhibition of Rho and GSK3 by their inhibitors Y27632 and SB216763, respectively, strongly raised E-cad, β-catenin and Slug. Dex decreased Y27632-mediated increase of β-catenin. Dex at 2.0 µM inhibited SB216763-regulated E-cad, β-catenin and slug. In conclusion, EMT in psoriatic keratinocytes may be defined as an intermediate phenotype of type 2 EMT. ERK, Rho and GSK3 play active roles in the process of EMT in psoriatic keratinocytes.

Indexed as

Epithelial-Mesenchymal TransitionAdultBiomarkersCase-Control StudiesEpidermisExtracellular Signal-Regulated MAP KinasesFemaleGene ExpressionGlycogen Synthase Kinase 3HumansImmunohistochemistryKeratinocytesMaleMiddle AgedPsoriasisrho GTP-Binding ProteinsBiomarkersExtracellular Signal-Regulated MAP KinasesGlycogen Synthase Kinase 3rho GTP-Binding ProteinsE-cadherinepithelial–mesenchymal transitionkeratinocytepsoriasisvimentin

Identifiers

PMID26269426
PMCPMC4554915
OpenAlexW2342319070

What OpenQuestion holds

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LicenceCC BY
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.