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N. Kato, S. Shimmura, T. Kawakita, H. Miyashita, K. Higa, S. Yoshida, Y. Ogawa, H. Okano, H. Okano, K. Tsubota; E-Cadherin Repression and Epithelial-Mesenchymal Transition in the Pathogenesis of Pterygium. Invest. Ophthalmol. Vis. Sci. 2007;48(13):5291.
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To investigate whether epithelial-mesenchymal transition (EMT) caused by E-cadherin repression is involved in the pathogenesis of pterygium.
Four eyebank corneas with intact pterygium and 9 surgically excised pterygial tissues were histopathologically assessed. Transmission electron microscopy was used to examine the ultrastructure of the pterygial head. Beta-catenin and E-cadherin expression were examined by immunohistochemistry. Epithelial cells undergoing EMT-like changes were identified by double immunostaining for alpha-smooth muscle actin (a-SMA)/ vimentin and cytokeratin 14. The expression of the transcriptional repressors of E-cadherin, Snail, Slug and SIP-1, were assessed by immunohistochemistry or semiquantitative PCR.
Histopathology showed aberrant fibrotic proliferation beneath the pterygium epithelium, with epithelial processes extending into the stroma. Transmission electron microscopy revealed the dissociation of epithelial cells, which were surrounded by activated fibroblast-like cells. Characteristic downregulation of E-cadherin and intranuclear accumulation of beta-catenin and lymphoid-enhancer-factor-1 in pterygial epithelium were also observed by immunohistochemistry. Epithelial cells extending into the stroma were positive for both a-SMA/ vimentin and cytokeratin 14. Snail and Slug were immunopositive in the nuclei of pterygial epithelial cells, but not in normal corneal epithelial cells. Real time-PCR showed increased expression of Snail and SIP-1 mRNA in pterygial epithelium.
EMT of basal epithelial cells caused by E-cadherin repression may play a key role in the pathogenesis of pterygium.
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