Yang Qin, Tan Qing Qing, Lan Chang Jun, Lv Bo Zhen, Zhou Gui Mei, Zhong Wei Qi, Gu Zhi Ming, Mao Yu Mei, Liao Xuan
Department of Ophthalmology, Affiliated Hospital of North Sichuan Medical College, Nanchong, China.
Department of Ophthalmology and Optometry, North Sichuan Medical College, Nanchong, China.
Front Physiol. 2021 Dec 23;12:790580. doi: 10.3389/fphys.2021.790580. eCollection 2021.
KCNQ5 is suggestively associated with myopia, but its specific role in the myopic process has not been studied further. The aim of this study was to investigate the expression of potassium channel gene KCNQ5 and the changes of K microenvironment within the retina of form deprivation myopia (FDM) guinea pigs. A total of 60 guinea pigs were randomly divided into the normal control (NC) group, the self-control (SC) group, and the form-deprivation (FD) group for different treatments. Molecular assays and immunohistochemistry (IHC) were conducted to measure the expression and distribution of KCNQ5-related gene and protein in the retina. We determined the K concentration in the retina. In addition, the possible effects of form deprivation on potassium ionic currents and the pharmacological sensitivity of KCNQ5 activator Retigabine and inhibitor XE991 to the M-current in RPE cells were investigated using the patch-clamp technique. As a result, FD eyes exhibited more myopic refraction and longer AL. The mRNA and protein levels of KCNQ5 significantly decreased in the FD eyes, but the K concentration increased. In addition, the M-type K current [IK] density decreased in FD RPE cells, and were activated or inhibited in a concentration-dependent manner due to the addition of Retigabine or XE991. Overall, KCNQ5 was significantly downregulated in the retina of FD guinea pigs, which may be associated with the increasing K concentration, decreasing IK density, and elongating ocular axis. It suggested that KCNQ5 may play a role in the process of myopia, and the intervention of potassium channels may contribute to the prevention and control of myopia.
KCNQ5与近视存在潜在关联，但其在近视进程中的具体作用尚未得到进一步研究。本研究旨在探究钾通道基因KCNQ5在形觉剥夺性近视（FDM）豚鼠视网膜中的表达及钾微环境的变化。总共60只豚鼠被随机分为正常对照组（NC）、自身对照组（SC）和形觉剥夺组（FD）进行不同处理。采用分子检测和免疫组织化学（IHC）方法来测量视网膜中KCNQ5相关基因和蛋白的表达及分布。我们测定了视网膜中的钾浓度。此外，运用膜片钳技术研究了形觉剥夺对钾离子电流的可能影响以及KCNQ5激活剂瑞替加滨和抑制剂XE991对视网膜色素上皮（RPE）细胞中M电流的药理敏感性。结果显示，FD组眼睛表现出更多的近视性屈光和更长的眼轴长度。FD组眼睛中KCNQ5的mRNA和蛋白水平显著降低，但钾浓度升高。此外，FD组RPE细胞中的M型钾电流[IK]密度降低，并且由于添加瑞替加滨或XE991而呈浓度依赖性激活或抑制。总体而言，FD豚鼠视网膜中的KCNQ5显著下调，这可能与钾浓度升高、IK密度降低和眼轴延长有关。这表明KCNQ5可能在近视进程中发挥作用，并且对钾通道的干预可能有助于近视的防控。
