Zhang Hengli, Wong Chun Lung, Shan Sze Wan, Li King Kit, Cheng Angela K, Lee Kam Len, Ge Jian, To Chi Ho, Do Chi Wai
State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, China.
Clin Exp Optom. 2011 Nov;94(6):528-35. doi: 10.1111/j.1444-0938.2011.00611.x. Epub 2011 Sep 5.
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.
实验证据表明，近视性和远视性光学离焦分别导致脉络膜增厚和变薄，使视网膜朝着焦点平面向前和向后移动；然而，这一现象的潜在机制仍不清楚。据推测，脉络膜厚度的变化可能是由跨视网膜色素上皮（RPE）的离子和液体转运改变引起的。因此，本研究的目的是确定正常未处理状态及晶状体诱导性近视状态下雏鸡RPE中特定Cl(-)转运体/通道mRNA和蛋白质的含量。
使用35只白来航雏鸡。通过在一只眼睛上固定一个-10D的透镜来诱导晶状体性近视，而对照眼安装平光镜。分别通过实时聚合酶链反应和蛋白质印迹法评估靶向Cl(-)转运体和通道的mRNA和蛋白质表达。
我们的结果表明，包括NKCC、CFTR、ClC-2、ClC-5、ClC-7和CLCA在内的几种Cl(-)转运体和通道的基因和蛋白质产物在雏鸡RPE中表达。佩戴-１０D透镜一天后，除了屈光出现近视性偏移和脉络膜变薄外，与对侧眼相比，近视眼中某些mRNA和蛋白质（例如NKCC）的含量也平行降低。治疗四天后，这些mRNA和蛋白质自发恢复到对照水平。
近视眼中Cl(-)转运体和通道表达的相对降低可能导致跨RPE的离子和液体转运减少，导致脉络膜变薄，并可能加速眼轴伸长。了解晶状体诱导性近视发展过程中所使用的Cl(-)转运机制，可能有助于开发通过影响RPE液体转运来控制近视进展的新方法。
