Overexpression of miR-153 promotes oxidative stress in MPP+-induced PD model by negatively regulating the Nrf2/HO-1 signaling pathway.

Increasing evidence points to oxidative stress as a chief mediator of Parkinson's disease (PD) characterized by progressive loss of dopamine neurons in the pars compacta of the substantia nigra. At present, microRNAs (miRNAs) have been recognized as important regulators in oxidative stress. Furthermore, miRNAs were also involved in the neuropathology of neurodegenerative disorders, including PD. In this study, we aimed to explore the influences of miR-153 and Nrf2 in oxidative stress during the development of PD. It was found that the expression of miR-13 and Nrf2 detected by qRT-PCR were significantly increased and decreased, respectively, in serum of PD patients and MPP+-induced SH-SY5Y cells. The target relationship between miR-153 and Nrf2 was determined by dual-luciferase assay. Moreover, after transfecting with miR-153 mimics and inhibitor, the expressions of Nrf2 in mRNA and protein were down-regulated and up-regulated, respectively. The indexes of oxidative stress were examined by biochemical methods. The data revealed that miR-153 could facilitate oxidative stress by negatively regulating Nrf2 in MPP+-treated SH-SY5Y cells. Finally, it was observed that miR-153 could suppress the Nrf2/HO-1 signaling pathway in MPP+-treated SH-SY5Y cells. Therefore, these findings indicated that overexpression of miR-153 could promote oxidative stress in PD by targeting the Nrf2/HO-1 signaling pathway, possibly providing a new way to treat PD. IJCEP