Down-regulation of miR-23a-3p protects retinal pigment epithelial cells from oxidative stress via inducing SRC-3-mediated autophagy

Age-related macular degeneration is a main degenerative eye disease that eventually brings out irreversible vision loss. This study aimed to unmask miR-23a-3p’s role in AMD along with its underlying mechanism. Through MTT assay and flow cytomery analysis, H 2 O 2 -treated ARPE−19 cells viability and apoptosis were measured. Oxidative stress and inflammation-related markers were assessed by commercial kits. ROS level were detected using DCFH–DA. Immunofluorescence was employed to analyze the LC3B fluorescence intensity. Using bioinformatics analysis and luciferase reporter assay, the molecular relationship between SRC-3 and miR-23a-3p was verified. MiR-23a-3p was gradually up-regulated in ARPE−19 cells in a H 2 O 2 dose-dependent pattern. MiR-23a-3p repressed H 2 O 2 -exposed ARPE−19 cells viability and autophagy while promoted cell apoptosis, oxidative stress, and inflammation. Pretreatment of 3-MA, autophagy inhibitor, could offset the impacts of miR-23a-3p repression on H 2 O 2 -treated ARPE−19 cells viability, apoptosis, oxidative stress, inflammation along with autophagy. SRC-3 was miR-23a-3p’s target mRNA. SRC-3 was gradually down-regulated in ARPE−19 cells in a H 2 O 2 dose-dependent way. SRC-3 expression was negatively modulated by miR-23a-3p. SRC-3 silencing reversed the impacts of miR-23a-3p repression on H 2 O 2 -treated ARPE−19 cells viability, apoptosis, oxidative stress, inflammation, along with autophagy. Down-regulation of miR-23a-3p prevents retinal pigment epithelial cells from oxidative stress through inducing SRC-3-mediated autophagy.