LncRNA MIAT Inhibits MPP+-Induced Neuronal Damage Through Regulating the miR-132/SIRT1 Axis in PC12 Cells.

Abstract

Parkinson's disease (PD) is an age-related neurodegenerative disease caused by the loss of dopaminergic neurons in the substantia nigra. LncRNA MIAT has been shown to be critical in Alzheimer's disease, but its role and mechanism in PD are still unknown. Differentiated PC12 cells were treated with 1-methyl-4-phenylpyridinium (MPP+) to establish in vitro cell injury model of PD. MTT, Annexin V-PI double staining test and Western blot were used to detect cell viability and apoptosis. Reactive oxygen species (ROS), superoxide dismutase (SOD) and phospholipid hydroperoxide glutathione peroxidase (GSH-PX) kits were used to evaluate oxidative stress in cells. These results showed that LncRNA MIAT was down-regulated in MPP+-induced PC12 cells. Overexpression of LncRNA MIAT remarkably increased cell viability, inhibited cell apoptosis and oxidative stress in MPP+-treated cells. In addition, we proved that miR-132 is a target of LncRNA MIAT. Overexpression of miR-132 could reverse the positive effect of LncRNA MIAT overexpression on MPP+-induced cell oxidative stress injury. SIRT1 is a target of miR-132 and silencing of SIRT1 attunated the positive effect of LncRNA MIAT overexpression on oxidative stress injury in MPP+-induced PC12 cells. In conclusion, this study indicated that LncRNA MIAT suppressed MPP+-induced oxidative stress injury by regulating miR-132/SIRT1 axis in PC12 cells.