OBJECTIVE: The present study aimed to explore the role and the underlying mechanism of miR-221 in Parkinson's Disease. MATERIALS AND METHODS: To perform our investigation, a PD cell model was created by using 6-OHDA. Cell viability and proliferation assays, and flow cytometry analysis were performed to detect cell viability and apoptosis. The qRT-PCR and western blotting were used for gene and protein level detection. RESULTS: We found that the expression of miRNA-221 is significantly lower in 6-OHDA treated PC12 pheochromocytoma cells compared to the normal cells. The results of further analysis indicated that miR-221 mimic significantly promoted the cell viability and proliferation of PC12 cells treated with 6-OHDA. MiR-221 mimic significantly inhibited 6-OHDA-treated PC12 cells from apoptosis. These effects were eliminated by PTEN over-expression. We also revealed that PTEN was a direct target gene of miR-221. Moreover, we found miR-221 mimic significantly promoted the phosphorylation of AKT in PC12 cells treated with 6-OHDA, and over-expression of PTEN could eliminate this effect. CONCLUSIONS: MiR-221 plays a protective role in Parkinson's Disease via regulating PC12 cell viability and apoptosis by targeting PTEN. Therefore, miR-221 may serve as a potential therapeutic target for Parkinson's disease treatment (Fig. 3, Ref. 27).
OBJECTIVE: The present study aimed to explore the role and the underlying mechanism of miR-221 in Parkinson's Disease. MATERIALS AND METHODS: To perform our investigation, a PD cell model was created by using 6-OHDA. Cell viability and proliferation assays, and flow cytometry analysis were performed to detect cell viability and apoptosis. The qRT-PCR and western blotting were used for gene and protein level detection. RESULTS: We found that the expression of miRNA-221 is significantly lower in 6-OHDA treated PC12pheochromocytoma cells compared to the normal cells. The results of further analysis indicated that miR-221 mimic significantly promoted the cell viability and proliferation of PC12 cells treated with 6-OHDA. MiR-221 mimic significantly inhibited 6-OHDA-treated PC12 cells from apoptosis. These effects were eliminated by PTEN over-expression. We also revealed that PTEN was a direct target gene of miR-221. Moreover, we found miR-221 mimic significantly promoted the phosphorylation of AKT in PC12 cells treated with 6-OHDA, and over-expression of PTEN could eliminate this effect. CONCLUSIONS:MiR-221 plays a protective role in Parkinson's Disease via regulating PC12 cell viability and apoptosis by targeting PTEN. Therefore, miR-221 may serve as a potential therapeutic target for Parkinson's disease treatment (Fig. 3, Ref. 27).