Glaucoma is a progressive optic neuropathy and is one of the leading causes of blindness in the industrialized countries. The involvement of microRNAs (miRs) has been implicated in regulating the complex biological responses to changes in intraocular pressure. However, the therapeutic role of miR-200a on glaucoma has not been well studied yet. In this study, we confirmed the role of miR-200a in glaucoma progression and identified the related mechanism. Microarray expression profiles were used to screen the glaucoma-related genes. The relationship between miR-200a and FGF7 was validated by bioinformatics analysis and dual-luciferase reporter gene assay. Glaucoma-related parameters including the expression of CD11b and iNOS, activation of Muller cells, and apoptosis of retinal ganglion cells (RGCs) in the mouse model were measured by immunohistochemistry, MTT assay and TUNEL assay, respectively. miR-200a was reduced in glaucoma, whereas FGF7 was robustly induced. Thereby, we speculated that FGF7 was negatively regulated by miR-200a. Downregulated miR-200a could activate the MAPK signaling pathway following elevations in ERK, JNK, p38 and Bax expression and reduction in Bcl-2 expression. In the mouse model, downregulated miR-200a increased the expression of CD11b and iNOS and the apoptosis of RGCs, but stimulated the inactivation of Muller cells. However, the above-mentioned alternations induced by downregulated miR-200a were reversed after FGF7 repression. miR-200a can inhibit the FGF7-mediated MAPK signaling pathway and play a protective role on improving the glaucoma-induced optical nerve injury.

青光眼是一种进行性视神经病变，是工业化国家失明的主要原因之一。microRNA（miRs）的参与已涉及调节对眼压变化的复杂生物学反应。但是，miR-200a对青光眼的治疗作用尚未得到很好的研究。在这项研究中，我们证实了miR-200a在青光眼进展中的作用，并确定了相关机制。微阵列表达谱用于筛选青光眼相关基因。miR-200a和FGF7之间的关系已通过生物信息学分析和双荧光素酶报告基因分析验证。青光眼相关参数包括CD11b和iNOS的表达，穆勒细胞的激活，分别通过免疫组织化学，MTT法和TUNEL法检测小鼠模型中视网膜神经节细胞（RGCs）的凋亡和凋亡。miR-200a在青光眼中减少，而FGF7被强烈诱导。由此，我们推测FGF7被miR-200a负调控。下调的miR-200a可以在ERK，JNK，p38和Bax表达升高以及Bcl-2表达降低后激活MAPK信号通路。在小鼠模型中，miR-200a的下调增加了CD11b和iNOS的表达以及RGC的凋亡，但刺激了Muller细胞的失活。然而，在FGF7抑制后，由miR-200a下调引起的上述交替被逆转。