Long non-coding RNA NEAT1 mediates the toxic of Parkinson's disease induced by MPTP/MPP+ via regulation of gene expression.

Parkinson's disease (PD) is a result of the loss of dopaminergic neurons in the substantia nigra and is expected to increase the economic burden on patients' families and societies. NEAT1, a long non-coding RNA, is known as a cancer-related gene, however, the role of it in PD remains unclear. The aims of this study are to detect the NEAT1-mediated effects in PD and explore the mechanism of NEAT1 in PD. One group (n = 6) of C57BL/6 model mice were intraperitoneal injected with 1-Methyl-4-phenyl-2, 3, 6-tetrahydropyridine (MPTP), while another group (n = 6) was treated with saline and served as control. Human neuroblastoma cell line SH-SY5Y was pretreated with 1-Methyl-4-phenylpyridinium (MPP+). Cell viability and apoptosis, as well as gene expression with different treatments were examined. Up-regulated NEAT1 was found in MPTP-induced PD mice. Moreover, the NEAT1 expression was positively correlated with the concentration of MPP+. In SH-SY5Y cells stimulated by MPP+, NEAT1 knockdown dramatically promoted cell viability and suppressed cell apoptosis. Additionally, down-regulation of NEAT1 also decreased the ratio of Bax/Bcl-2, the activity of caspase-3, as well as the expression of α-synuclein. Moreover, α-synuclein overexpression could significantly reverse the increase in cell viability and the decrease in cell apoptosis induced by NEAT1 knockdown. The results suggested that the knockdown of NEAT1 will have a protective effect on MPTP-induced PD mice. The mechanism may be related to the dysregulation of α-synuclein.