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Experimental evidence has shown that myopic and hyperopic optical defocus induces thickening and thinning of the choroids, respectively, moving the retina forward and backward toward the plane of focus; however, the underlying mechanism of this phenomenon remains elusive. It has been hypothesised that the change in choroidal thickness might be elicited by the alteration of ion and fluid transport across the retinal pigment epithelium (RPE). Therefore, the aims of the present study were to determine the content of specific Cl- transporter/channel mRNA and proteins in chick RPE in a normal, untreated state and in lens-induced myopia.Thirty-five White Leghorn chicks were used. Lens-induced myopia was achieved by securing a -10 D lens in one eye, while the control eye was mounted with a plano lens. The mRNA and protein expression of the targeted Cl- transporter and channels were assessed by real-time polymerase chain reaction and western blot, respectively.Our results showed that the gene and protein products of several Cl- transporter and channels including NKCC, CFTR, ClC-2, ClC-5, ClC-7 and CLCA were expressed in young chick RPE. After one day of -10 D lens wear, in addition to the myopic shift in refraction and choroidal thinning, there was a parallel reduction in content of some mRNAs and proteins (for example, NKCC) in the myopic eye compared with the fellow eye. Spontaneous recovery of these mRNAs and proteins to control levels was demonstrated after four days of treatment.The relative reduction of Cl- transporter and channel expression in the myopic eye might cause a decrease in ion and fluid transport across the RPE, leading to a thinning of the choroid and potentially accelerating axial elongation. Understanding of the identity of the Cl- transport machinery used in developing lens-induced myopia might facilitate development of novel approaches for controlling myopic progression by influencing fluid transport by the RPE.