This study aimed to clarify the regulation role of miR-708 and miR-335-3p in retinal ganglion cell (RGC) autophagy and apoptosis in glaucoma. Chronic glaucoma mice were established by laser photocoagulation. RGCs were isolated and transfected with a series of plasmids and the cultured in 60 mmHg pressure. miR-335-3p, miR-708, and ATG3 mRNA expressions were detected by qRT-PCR. Protein levels of ATG3, autophagy-related protein LC3, and p62 were detected by Western blot. The apoptosis of RGCs was detected by flow cytometry. The regulation role of miR-335-3p/miR-708 in ATG3 was confirmed by the dual-luciferase reporter gene. The expressions of several miRNAs were measured in retinal tissues from chronic glaucoma mice and RGCs under pressure conditions, and results showed that both miR-335-3p and miR-708 were down-regulated. Besides, the inhibition of miR-708 and miR-335-3p induced the apoptosis of RGCs through promoting autophagy. Also, miR-708 and miR-335-3p could bind to ATG3 and targeted regulated ATG3. Furthermore, the interference with miR-708/miR-335-3p induced RGC apoptosis by up-regulating ATG3 to promote autophagy. In general, the down-regulation of miR-708 and miR-335-3p contributed to the apoptosis of RGCs through promoting autophagy in glaucoma.

本研究旨在阐明miR-708和miR-335-3p在青光眼视网膜神经节细胞（RGC）自噬和凋亡中的调控作用。通过激光光凝法建立慢性青光眼小鼠。RGC 被分离并用一系列质粒转染，并在 60 mmHg 压力下培养。通过qRT-PCR检测miR-335-3p、miR-708和ATG3 mRNA的表达。通过蛋白质印迹检测 ATG3、自噬相关蛋白 LC3 和 p62 的蛋白质水平。流式细胞术检测RGCs的凋亡。双荧光素酶报告基因证实了 miR-335-3p/miR-708 在 ATG3 中的调节作用。在压力条件下测量了慢性青光眼小鼠和 RGCs 视网膜组织中几种 miRNA 的表达，结果显示 miR-335-3p 和 miR-708 均下调。除了，抑制 miR-708 和 miR-335-3p 通过促进自噬诱导 RGCs 凋亡。此外，miR-708 和 miR-335-3p 可以与 ATG3 结合并靶向调节 ATG3。此外，干扰 miR-708/miR-335-3p 通过上调 ATG3 促进自噬诱导 RGC 凋亡。总的来说，miR-708和miR-335-3p的下调通过促进青光眼自噬促进了RGCs的凋亡。