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Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Open+Biol 2015 ; 5 (8): ä Nephropedia Template TP
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Analysis of epithelial?mesenchymal transition markers in psoriatic epidermal keratinocytes #MMPMID26269426
Man XY; Chen XB; Li W; Landeck L; Dou TT; Chen Jq; Zhou J; Cai SQ; Zheng M
Open Biol 2015[Aug]; 5 (8): ä PMID26269426show ga
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-?1 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, ?-catenin, Slug and ?5 integrin. Moreover, inhibition of Rho and GSK3 by their inhibitors Y27632 and SB216763, respectively, strongly raised E-cad, ?-catenin and Slug. Dex decreased Y27632-mediated increase of ?-catenin. Dex at 2.0 µM inhibited SB216763-regulated E-cad, ?-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.