LncRNA OIP5-AS1 reduces α-synuclein aggregation and toxicity by targeting miR-126 to activate PLK2 in human neuroblastoma SH-SY5Y cells

It has been reported that many long noncoding RNAs (lncRNA) are abnormally expressed in Parkinson's disease (PD). However, the knowledge about the role of dysregulated lncRNA in the pathological process of PD and the potential molecular regulation mechanism is still limited. Our immunofluorescence data show that miR-126 enhances the aggregation and toxicity of synuclein, while lncRNA OIP5-AS1 reduces the aggregation and toxicity of MPP + induced alpha-synuclein by targeting miR-126. Luciferase experiments have found that miR-126 regulates alpha-synuclein by targeting PLK2. Western blot and IP experimental analysis showed that this process is achieved by regulating PLK2/alpha-synuclein autophagy. In conclusion, our data indicate that OIP5-AS1 promotes the autophagy of PLK2-alpha-synuclein by targeting the miR-126 axis with pathogenic factors, thus reducing the aggregation toxicity of alpha-synuclein, which It will help better to understand the mechanism of dopaminergic neuron loss in PD and provide novel treatment options.

Automated summary

The study indicates that OIP5-AS1 promotes autophagy of PLK2-alpha-synuclein by targeting the miR-126 axis, reducing the aggregation toxicity of alpha-synuclein. This mechanism helps understand dopaminergic neuron loss in Parkinson's disease and offers potential novel treatment options.