miR-486 inhibits PM2.5-induced apoptosis and oxidative stress in human lung alveolar epithelial A549 cells.

Background: Environmental exposure to particulate matter 2.5 (PM2.5) threatens public health, which has caused worldwide concerns. MicroRNAs (miRNAs, miRs) participate in multiple biological regulation. Among them, miR-486 has been reported to be a beneficial molecule for cell survival in various cell types. However, the potential function of miR-486 in PM2.5-induced cytotoxic is still uncertain. Methods: The expression of miR-486 was detected by quantitative real-time polymerase chain reaction (qRT-PCR) after A549 cells incubated with PM2.5. Then TUNEL staining and DCFH-DA fluorescence were used to test the apoptosis and ROS generation of A549 cells after exposed to PM2.5 with miR-486 mimic. Western blot was performed to determine the expression of Bax/Bcl2 ratio. In addition, western blot and rescue experiments were conducted to determine the target gene of miR-486. Results: After treated with PM2.5, the expression of miR-486 was decreased. And miR-486 mimic treatment reduced cell apoptosis and reactive oxygen species (ROS) generation induced by PM2.5 exposure. Further studies showed that miR-486 negatively regulated the protein levels of PTEN and FOXO1. Rescue experiments demonstrated that PTEN and FOXO1 mediated the protective effects of miR-486 in PM2.5-treated human lung alveolar epithelial A549 cells. Conclusions: Collectively, our findings identify that miR-486 relieves PM2.5-induced cell injury by targeting PTEN and FOXO1 in human lung alveolar epithelial A549 cells.