强光信号通过视网膜调控眼球生长与近视眼发生机制研究

Our recent research indicated that light and defocus could regulate emmetropization in primates. In this program, based on lens-induced myopia animal model, we try to dynamically observe the effect of high ambient lighting on refractive state in rhesus monkeys and systematically analyze the expression of crystalline, Nos, NDRG-1, Egr-1 in retinal amacrine cells, bipolar cells, and photoreceptor cells, which have been proved to be related to defocus. We also isolate and purify retinal proteins, identify high ambient lighting and defocus target proteins in retina, and therefore further understand the biologic functions of crystalline, Nos, NDRG-1, Egr-1. Our systematic research on proteinic basis of myopia generation as well as its development could give clues at early response gene and functional proteomics level to possible mechanisms, which might be responsible for the generation and development of myopia. Furthermore, our research could also provide totally new theoretic basis and methods for myopia prevention and treatments.

申请者最近的研究表明,光觉和形觉信号联合可调控恒河猴眼正视化过程,在近视眼发生发展过程中起重要作用，但光觉信号的调控机制还不清楚。本项目拟用动态观察、分子探针和蛋白质时空效应等研究方法，探讨强光信号作用下，恒河猴眼球生长和屈光状态发育过程以及视网膜无长突细胞、双极细胞和光感受器细胞crystalline, Nos, NDRG-1, Egr-1 及其相关蛋白之间的相互作用关系，寻找影响或抑制蛋白相互作用的因素，了解强光信号影响眼轴延长、屈光状态变化过程及其调控，从而进一步了解近视眼发生、发展的可能机制,为近视眼的防治提供新的理论依据和方法。

本项目用动态观察、分子探针和蛋白质时空效应等研究方法，探讨强光信号作用下，恒河猴眼球生长和屈光状态发育过程以及视网膜无长突细胞、双极细胞和光感受器细胞crystalline、Nos、NDRG-1、Egr-1及其相关蛋白之间的相互作用关系。结果发现：1）强光觉信号和自然光作用通过减少玻璃体腔长度的延长，明显减缓近视发展；2）强光觉信号和自然光作用下，可能通过影响视网膜组织代谢水平调控近视发生发展；3）强光觉信号和自然光作用下，可能通过引起视网膜组织基因转录水平和表观遗传学的改变,调控恒河猴眼球生长和屈光状态发育过程。本项目进一步明晰了强光觉信号和自然光作用减缓近视眼发展的可能机制，为近视眼的预防和治疗提供了新的理论依据和方法。