September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Acceleration of EGF expression and related cell behaviors induced by travoprost were cancelled by further addition of an EGF receptor inhibitor in corneal epithelium
Author Affiliations & Notes
  • Yukihisa Takada
    Wakayama Medical University, Wakayama, Wakayama, Japan
  • Osamu Yamanaka
    Wakayama Medical University, Wakayama, Wakayama, Japan
  • Takayoshi Sumioka
    Wakayama Medical University, Wakayama, Wakayama, Japan
  • Yuka Okada
    Wakayama Medical University, Wakayama, Wakayama, Japan
  • Shizuya Saika
    Wakayama Medical University, Wakayama, Wakayama, Japan
  • Footnotes
    Commercial Relationships   Yukihisa Takada, None; Osamu Yamanaka, None; Takayoshi Sumioka, None; Yuka Okada, None; Shizuya Saika, None
  • Footnotes
    Support  none
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 1251. doi:
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      Yukihisa Takada, Osamu Yamanaka, Takayoshi Sumioka, Yuka Okada, Shizuya Saika; Acceleration of EGF expression and related cell behaviors induced by travoprost were cancelled by further addition of an EGF receptor inhibitor in corneal epithelium. Invest. Ophthalmol. Vis. Sci. 2016;57(12):1251.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : To examined the effects of epidermal growth factor (EGF) receptor inhibitor, PD168393 (PD), on corneal epithelium treated with travoprost. We previously reported that travoprost induced the proliferation of corneal epithelial cells with increased expression of EGF in vitro and in organ-culture of a mouse cornea (ARVO2015).

Methods : Human corneal epithelial cells (HCE) were cultured for 24 hrs in the presence or absence of travoprost (0.04 g/l) and/or PD (10μM). We examined expression of E-cadherin by using immunohistochemistry and cell proliferation by Alamar blue assay. Mouse eyeball was organ-cultured for 48h in the presence or absence of travoprost and/or PD. Expression of EGF, Ki67, phosphorylated (p) -beta catenin and adhesion molecules (E-cadherin, p-FAK) and signal pathway related with EGF (pErk, pSmad3) in corneal epithelium was immunohistochemically examined.

Results : PD blocked travoprost promotion of cell proliferation and E-cadherin expression in the cultured cells. Promotion of expression of EGF, Ki 67, p-beta catenin, E-cadherin, p-FAK by travoprost in corneal epithelium of an organ-cultured mouse eye was counteracted by further addition of PD. Travoprost induced phosphorylation of Erk and Smad3, that was also canceled by adding PD.

Conclusions : Acceleration of EGF expression and related cell behaviors, i.e., promotion of cell proliferation, adhesion molecule expression, signaling activation, by adding travoprost to corneal epithelial cell culture or organ-cultured corneal epithelium were cancelled by further addition of PD. Control of EGF signal could be a strategy to prevent travoprost-induced corneal epithelial disorder.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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