MicroRNA-181c functions as a protective factor in a 1-methyl-4-phenylpyridinium iodide-induced cellular Parkinson’s disease model via BCL2L11

M. Wei, L.-J. Cao, J.-L. Zheng, L.-J. Xue, B. Chen, F. Xiao, C.-S. Xu

Department of Neurology, Huai’an First People’s Hospital, Nanjing Medical University, Huai’an, Jiangsu Province, China. xuchangsong0103@163.com

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• Neurology

OBJECTIVE: Parkinson is one of the most common neurodegenerative diseases. At present, many studies have pointed out that miRNAs play a very important role in Parkinson’s development and process. MiR-181c has been shown to have a significant low expression in blood samples and brain tissues of Parkinson’s patients.

MATERIALS AND METHODS: We used 1-Methyl-4-Phenylpyridinium Iodide (MPP(+)) as a tool for constructing the Parkinson’s cell model, using mir181c mimics to construct an experimental model of acquisition. The cell viability of PC12 was detected by MTT and CCK8. Reactive oxygen species (ROS) and caspase-3 activity were analyzed. The apoptosis of PC12 was detected by flow cytometry (FCM), and luciferase was used to study the binding of target genes. The protein levels of BCL2L11were measured by Western-blot.

RESULTS: There was a significant low expression of mir181c in MPP(+)-morbid cells. PC12 cell viability was rescued by miR-181c overexpression. Flow cytometry showed that apoptosis in PC12 cells overexpressing miR-181c was significantly decreased. Also, ROS and caspase-3 activity were significantly decreased. Luciferase experiments showed that miR-181c may bind to the 3-’UTR side of BCL2L11 and inhibited its expression. By Western-blot, the BCL2L11 level was markedly decreased by miR-181c.

CONCLUSIONS: miR-181c could promote the cell viability and inhibit the apoptosis of PC12 cells induced by MPP (+) by downregulating BCL2L11, which may play a protective role and provide a new target for PD drug resistance research.

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