Characterization of Cl- Transporter and Channels in Lens-Induced Myopic Eyes

Abstract

Purpose: : Experimental evidence has shown that myopic and hyperopic defocuses induce choroidal thickening and thinning, respectively. The underlying mechanism of this phenomenon is unclear but has been implicated in myopia development. It is possible that the changes in choroidal thickness are elicited by the alternation of ion and fluid transport across retinal pigment epithelium (RPE) which plays important role in relaying growth signals from neural retina to choroid. The aim of this study are to (1) to determine the presence of specific Cl^- transporter and channels in chick RPE and (2) to identify the molecular candidates and their expression profiles in lens-induced myopia.

Methods: : White Leghorn chicks were used. Lens-induced myopia was achieved by securing a -10D lens in one eye while the fellow eye (mounted with a plano lens) was used as control. The mRNA and protein expression of these Cl^- transporter and channels were assessed by real-time PCR and Western blot, respectively.

Results: : The gene and protein products of several Cl^- transporter and channels including NKCC, CFTR, ClC-2, ClC-5, ClC-7, and CLCA expressed in chick RPE. After 1 day of -10D lens wear, there was a parallel down-regulation of these genes and proteins in myopic eye as compared to contralateral fellow eye. After 4 days of lens treatment, spontaneous recoveries of some genes but not proteins were observed in myopic eye compared with control eye.

Conclusions: : The differential expression profiles between myopic and control eye may suggest a physiological role for Cl^- transport modulation in RPE for myopic growth. The understanding of the identity of the Cl^- transport machinery used in developing lens-induced myopia may facilitate the design of pharmacologic strategies for controlling myopia progression by influencing the signal-mediated fluid transport by RPE.

Keywords: myopia • retinal pigment epithelium • ion channels