MicroRNA-106a regulates the apoptosis and oxidative stress of porcine trabecular meshwork cells by targeting FAS.

This study investigates the impact of miR-106a on trabecular meshwork (TM) and its potential molecular mechanism, as TM dysfunction due to decreased cell viability is a major pathological feature of POAG. Primary porcine TM (PTM) cells were isolated and exposed to hyperoxic conditions to induce senescence. Through small RNA sequencing and qPCR verification, miR-106a was downregulated in aging PTM cells. The transfection system overexpressing miR-106a in PTM cells was achieved by polydopamine (PDA)/polyethyleneimine (PEI) nanoparticles (PDA/PEI NPs). Proliferation, apoptosis, and antioxidant capacity of PTM cells under normal and HO-treated conditions were assessed using CCK-8, mitochondrial assays, and reactive oxygen species measurements. As a result, Overexpression of miR-106a boosted PTM cell proliferation, dampened apoptosis, and enhanced capacity of antioxidative stress. Western blots were carried out to detect the expression of target genes of miR-106a. Mechanically, the expression of the two predicted target genes, FAS and CASP10, and genes of FAS-mediated signaling pathway were suppressed under normal and oxidative stress conditions. Dual-luciferase reporter results confirmed a direct binding between miR-106a and FAS. Thus, miR-106a promotes PTM cells' viability, suppresses apoptosis and enhances antioxidative stress capacity by targeting FAS in PTM cells. Therefore, our study provides a potential therapeutic target in glaucoma.