Silencing of <scp>miR</scp>‐497‐5p inhibits cell apoptosis and promotes autophagy in Parkinson's disease by upregulation of <scp>FGF2</scp>
Wenjie Zhu, Hui Zhang, Jun Gao, Xu Yun
Abstract
Abstract Parkinson's disease (PD) is a progressive neurodegenerative disorder with increasing prevalence in elderly individuals globally. MicroRNAs (miRNAs) have been confirmed to participate in the pathogenesis of various neurodegenerative diseases, including PD. MiR‐497‐5p is previously reported to be upregulated in PD. The present study was designed to further explore the function of miR‐497‐5p in PD. MiR‐497‐5p was significantly upregulated in 1‐methyl‐4‐phenylpyridinium (MPP + )‐treated SH‐SY5Y cells. Inhibition of miR‐497‐5p suppressed the cell apoptosis and triggered autophagy of MPP + ‐treated SH‐SY5Y cells. Further, miR‐497‐5p targeted fibroblast growth factor‐2 (FGF2) in MPP + ‐treated SH‐SY5Y cells. Subsequently, rescue assays revealed that miR‐497‐5p regulated apoptosis and autophagy of MPP + ‐treated SH‐SY5Y cells by mediation on FGF2. In addition, 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) induced PD mice models were established. The results exhibited that silencing of miR‐497‐5p improved mice bradykinesia, reduced cell apoptosis and induced autophagy in PD mice by FGF2. In conclusion, silencing of miR‐497‐5p alleviates PD by suppressing cell apoptosis and promoting autophagy in a FGF2 dependent manner, which will provide a novel target for Parkinson's disease management.