Long Noncoding RNA Maternally Expressed Gene 3 Targets miR-30b and Regulates the AKT Serine/Threonine Kinase 1/Phosphoinositide 3-Kinase Signaling Pathway of H2O2-Induced Proliferation, Apoptosis, and Oxidative Stress in Retinal Ganglion Cells

Oxidative stress is an important factor affecting retinal ganglion cell (RGC) apoptosis. RGC apoptosis is the main pathophysiological feature of visual impairment as a result of glaucoma. Recently, it has been found that long noncoding RNA (lncRNA) and microRNAs are involved in RGC apoptosis. Here, the function of lncRNA maternally expressed gene 3 (MEG3) and miR-30b in H2 O2-induced RGC proliferation, apoptosis, and oxidative stress was investigated. The expression levels of MEG3 and miR-30b were detected by RT-PCR; the effects of MEG3 and miR-30b on the proliferation and apoptosis of RGCs were observed by flow cytometry; the levels of apoptosis-related proteins and AKT/PI3K signal pathway proteins were detected by protein immunoassay; and the regulation of miR-34a by pvt1 was verified by in vivo and in vitro experiments. The expression of MEG3 and miR-30b increased and decreased significantly in RGCs treated by H2O2. MEG3 expression decreased, apoptosis level-related proteins decreased, the apoptosis rate reduced, and the activity of MDA and SOD decreased. When the expression of miR-34a was inhibited, the proliferation rate of RGCs increased, the apoptosis rate decreased, and the level of apoptosis-related proteins decreased, which reversed MEG3’s effect on RGC apoptosis and proliferation. Furthermore, pvt1 could bind the miR-30b promoter and regulate it with in vitro expression and in vivo expression. Besides, we found that miR-30b can regulate the AKT/PI3K signaling pathway and participate in cell apoptosis and hyperplasia in stress response. LncRNA MEG3 targets miR-30b and regulates the AKT/PI3K signaling pathway on H2 O2-induced cell apoptosis, hyperplasia, and oxidative stress of RGCs.