Analysis of epithelial–mesenchymal transition markers in psoriatic epidermal keratinocytes |
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Authors: | Xiao-Yong Man Xi-Bei Chen Wei Li Lilla Landeck Ting-Ting Dou Jia-qi Chen Jiong Zhou Sui-Qing Cai Min Zheng |
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Institution: | 1.Department of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People''s Republic of China;2.Department of Dermatology, Ernst von Bergmann General Hospital, Teaching Hospital of Charité–University, Potsdam, Germany |
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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. |
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Keywords: | epithelial– mesenchymal transition psoriasis keratinocyte E-cadherin vimentin |
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