Abstract
Purpose :
To examine the effects of travoprost, an ingredient of prostaglandin-glaucoma eye drop, on ZO-1 expression in cultured corneal epithelial cells. We previously reported that travoprost upregulates expression of epidermal growth factor ( EGF ) and induced cell proliferation in cultured corneal epithelial cells and epithelium of an organ-cultured mouse cornea. Such effects of travoprost were cancelled by further addition of PD168393 ( PD ), an EGF receptor inhibitor ( ARVO2016 ).
Methods :
Human corneal epithelial cells ( HCEC ) were cultured for 24 hrs in the presence or absence of travoprost ( 0.04 g/l ) and/or PD ( 10 μM ). Expression of ZO-1 was evaluated by using immunocytochemistry and western blotting. Mouse eyeball was organ-cultured for 48h in the presence or absence of travoprost and/or PD. We examined expression of zo-1 in HCEC and in an organ-cultured mouse eyes by using immunohistochemistry.
Results :
Adding travoprost impaired cell-cell contact localization of ZO-1 and its protein expression in cultured cells. Further addition of PD canceled disturbance of normal localization of ZO-1, but did not reverse the suppression of its protein expression. In the organ-culture, adding travoprost reduced the expression level of ZO-1 in corneal epithelium and such suppression was reversed by further addition of PD.
Conclusions :
Travoprost down-regulated ZO-1 cell-cell adhesion, and the effect of travoprost was canceled by further addition of PD in cultured corneal epithelial cells and epithelium of an organ-cultured mouse cornea. Upregulation of EGF by travoprost (ARVO 2016) could explain the mechanism of the current data of expression pattern modulation of ZO-1 with travoprost with or without PD. The findings might explain the additional mechanism of travoprost-related corneal epithelial disorders.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.