Conclusion
LncRNA PART1 could alleviate the damage effects of MPP+ on SH-SY5Y cells by regulating microRNA-106b-5p/MCL1 axis, suggesting the potential therapeutic value of LncRNA PART1 as a target in PD.
Methods
An in vivo MPTP-induced mouse model of PD was generated and the SH-SY5Y cells were treated with MPP+ to induce neuronal damage in vitro. The expressions of LncRNA PART1 and microRNA-106b-5p were assessed by RT-qPCR. The level of caspase 3 protein was detected by western blot. CCK8 assay and Annexin V/PI staining were used for detecting cell viability and survival rate, respectively. The interactions between microRNA-106b-5p and LncRNA PART1 or MCL1 were determined by RNA pull-down assay, RIP assay and DLR assay. The levels of inflammatory cytokines were assessed by ELISA, and the levels of LDH, ROS or SOD were verified using the appropriate assay kits.
Objective
Parkinson's disease (PD) is a neurodegenerative disease caused by the loss of dopaminergic neurons. Here, we aimed to explore the function of LncRNA PART1 in PD and its underlying mechanisms.
Results
The expression of LncRNA PART1 was decreased in PD model in vivo and in vitro (all P<0.05). In SH-SY5Y cells treated with MPP+, the overexpression of LncRNA PART1 increased cell viability and reduced cell apoptosis, the secretion of inflammatory cytokines and oxidative stress reaction (all P<0.05). Furthermore, LncRNA PART1 sponged microRNA-106b-5p which directly targeted MCL1 and thus regulated the expression of MCL1. LncRNA PART1 attenuated the injury of SH-SY5Y cells induced by MPP+ via targeting microRNA-106b-5p and enhancing MCL1 expression.