OPTN基因是POAG的致病基因。OPTN( E50K)突变可以通过CREB通路下调BDNF的表达，进而诱发RGCs凋亡，导致青光眼的发生，但具体机制不清。在CREB通路中miR-9通过调节REST影响BDNF的表达；基因相关miRNA分析：miR-9与OPTN具有极高相关性。本研究拟利用已建立的体内外OPTN((E50K)突变转基因模型，过表达或抑制miR-9，观察OPTN(E50K)突变能否通过影响miR-9的表达水平进而影响CREB-REST通路调控BDNF表达及这种作用是否参与了OPTN（E50K）突变导致的RGC凋亡，阐明miR-9在OPTN（E50K）突变导致的青光眼中的作用，探寻与青光眼发病有关的miRNA，为临床早期诊断青光眼提供新的分子标志和药物治疗靶点；为青光眼基因治疗奠定基础。

OPTN is the POAG related gene, and the mutant E50K OPTN downregulates the expression of BDNF via CREB pathway, induces the apoptosis of RGCs, thus contributes to glaucoma, while the mechanism is still unclear. Given miR-9 regulating REST to alter the expression of BDNF in the CREB pathway, and it is highly related to OPTN in the miRNA analysis, our research is to overexpress and inhibit miR-9 in the vitro and vivo mutant E50K OPTN transgenic models to observe that mutant E50K OPTN whether alters CREB-REST pathway regulating expression of BDNF via impacting the level of miR-9, and induces the RGC apoptosis, in order to clarify the effect of miR-9 in the mutant E50K OPTN contributing to glaucoma, and seek the glaucoma related miRNA, provide new molecular marker for early diagnosis and drug target point for treatment, and establish the foundation for gene therapy of glaucoma.