Upregulation of miR‐200a and miR‐204 in MPP + ‐treated differentiated PC12 cells as a model of Parkinson’s disease

Background Parkinson's disease (PD) is ranked as the second most common neurodegenerative disorder caused by loss of dopaminergic neurons in the substantia nigra. Micro(mi)RNAs are a class of small noncoding RNAs that regulate gene expression and aberrant expression of them is closely correlated with many neurodegenerative conditions including PD. Silent information regulator 1 ( SIRT1 ) as a known deacetylase and B‐cell lymphoma‐2 ( BCL2 ) as an antiapoptotic factor play vital roles in neural protection and survival. Methods Differentiated PC12 cells exposed to MPP + were served here as a known PD model. Cell viability was determined by MTS assay. Apoptotic cells and ROS levels were detected using flow cytometry. Gene selection and miRNA–mRNA interaction analysis were performed through in silico methods. Relative expression of miRNAs and genes was examined by RT‐qPCR. Results MPP + exposure markedly reduced cell viability, enhanced oxidative stress, and induced apoptosis in differentiated PC12 cells. Sirt1 and BCL2 were shown to be markedly declined in response to MPP + , while miR‐200a and miR‐204 were significantly upregulated. Conclusion The first novel finding of the current study is altered expression of miR‐200a and miR‐204 in differentiated PC12 cells in response to MPP + , suggesting that deregulation of them participate in MPP + neurotoxicity mechanisms, possibly via affecting the expression of Sirt1 and BCL2 as potential targets.