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. 2011 Apr 14;52(5):2437-43.
doi: 10.1167/iovs.10-5635.

TGF-β induces sustained upregulation of SNAI1 and SNAI2 through Smad and non-Smad pathways in a human corneal epithelial cell line

Keiichi Aomatsu  1 , Tokuzo Arao, Koji Sugioka, Kazuko Matsumoto, Daisuke Tamura, Kanae Kudo, Hiroyasu Kaneda, Kaoru Tanaka, Yoshihiko Fujita, Yoshikazu Shimomura, Kazuto Nishio
Affiliations

TGF-β induces sustained upregulation of SNAI1 and SNAI2 through Smad and non-Smad pathways in a human corneal epithelial cell line

Keiichi Aomatsu et al. Invest Ophthalmol Vis Sci. .

Abstract

Purpose: The aim of this study was to investigate the expression changes of epithelial mesenchymal transition (EMT)-related molecules induced by TGF-β signaling in a human corneal epithelial cell line (HCECs).

Methods: The cellular response to TGF-β was evaluated by immunoblotting, quantitative real-time RT-PCR, and immunofluorescence microscopy in HCECs.

Results: TGF-β significantly increased mRNA expression of SNAI1, SNAI2, VIM, and FN1, but not TWIST1 through Smad and non-Smad pathways in HCECs. Protein expression of a mesenchymal marker N-cadherin was dose-dependently increased and that of an epithelial marker of E-cadherin was decreased by TGF-β. TGF-β, but not EGF, mediated the EMT-like morphologic changes. Both TGF-β and EGF were capable of upregulating SNAI1 and SNAI2 by about two-fold within a short response time. However, a detailed time course analysis revealed drastically different expression patterns, with TGF-β mediating a sustained upregulation of SNAI1 and SNAI2 for at least for 6 days and EGF allowing a return to the baseline expression values after 8 ∼ 12 h. These data indicate that TGF-β, but not EGF, induces sustained upregulation of SNAI1 and SNAI2 in HCECs.

Conclusions: TGF-β induces sustained upregulation of SNAI1 and SNAI2 through Smad and non-Smad pathways, EMT-like morphologic changes, downregulation of E-cadherin, and upregulation of N-cadherin in HCECs. The authors' findings provide insight into the TGF-β signaling and the temporal expression patterns of EMT-inducible transcription factors in HCECs.

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