Analysis of epithelial-mesenchymal transition markers in psoriatic epidermal keratinocytes.
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.
Department of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People's Republic of China manxy@zju.edu.cn.
Xiao-Yong
XY
Man
Department of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People's Republic of China.
Xi-Bei
XB
Chen
Department of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People's Republic of China.
Wei
W
Li
Department of Dermatology, Ernst von Bergmann General Hospital, Teaching Hospital of Charité-University, Potsdam, Germany.
Lilla
L
Landeck
Department of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People's Republic of China.
Ting-Ting
TT
Dou
Department of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People's Republic of China.
Jia-Qi
JQ
Chen
Department of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People's Republic of China.
Jiong
J
Zhou
Department of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People's Republic of China.
Sui-Qing
SQ
Cai
Department of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, People's Republic of China minz@zju.edu.cn.
Min
M
Zheng
D000328:Adult; D015415:Biomarkers; D016022:Case-Control Studies; D004817:Epidermis / Q000378:metabolism* / Q000473:pathology*; D058750:Epithelial-Mesenchymal Transition; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D015603:Keratinocytes / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D011565:Psoriasis / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D020741:rho GTP-Binding Proteins / Q000378:metabolism
D015415:Biomarkers; D048049:Extracellular Signal-Regulated MAP Kinases; D038362:Glycogen Synthase Kinase 3; D020741:rho GTP-Binding Proteins
E-cadherin; epithelial–mesenchymal transition; keratinocyte; psoriasis; vimentin