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10.1098/rsob.150032

http://scihub22266oqcxt.onion/10.1098/rsob.150032
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C4554915!4554915!26269426
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suck abstract from ncbi


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pmid26269426      Open+Biol 2015 ; 5 (8): ä
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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.
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