MicroRNA-216a inhibits neuronal apoptosis in a cellular Parkinson’s disease model by targeting Bax

• DOI: 10.1007/s11011-020-00546-x
• Publication Date: 2020-03-05T08:02:51Z
• Authors: Xiaobo Yang; Meng Zhang; Meng Wei; Anqi Wang; Yongning Deng; Hongmei Cao
• Keywords: Membrane Potential, Mitochondrial; Neurons; 0301 basic medicine; Dopaminergic Neurons; Apoptosis; Parkinson Disease; MicroRNAs; 03 medical and health sciences; Cell Line, Tumor; Humans; Reactive Oxygen Species; Signal Transduction; bcl-2-Associated X Protein

The study found that microRNAs play an important role in Parkinson's disease (PD). However, the function of MicroRNA-216a (miR-216a) in PD is unclear. Therefore, this experiment aimed to investigate the pathogenesis of miR-216a in PD. Using the toxicity of MPP+ to polyhexamine neurons, apoptosis of SH-SY5Y neuroblastoma cells was induced at different time by MPP+ to construct a stable acute PD cell model. The effects of DNA breakage, mitochondrial membrane potential (A ^ m), caspase-3 activity and nucleosome enrichment on cell apoptosis were detected by flow cytometry, TUNEL. MPP+ increased the toxic effects of dopaminergic neurons in a PD model. The introduction of miR-216a inhibited MPP + -induced neuronal apoptosis. The main manifestations were the decreased levels of positive rate of Tunel cells, caspase 3 activity and nucleosome enrichment factor. Bax was a direct target of miR-216a. In addition, Bax overexpression reversed the effects of miR-216a on neural cells. Bax downstream factors were also involved in miR-216a regulation of MPP + -triggered neuronal apoptosis. miR-216a regulated the progression of PD by regulating Bax, and miR-216a may be a potential target for PD.