期刊
ANNALS OF TRANSLATIONAL MEDICINE
卷 9, 期 10, 页码 -出版社
AME PUBL CO
DOI: 10.21037/atm-21-1613
关键词
SNHG1; miR-216a-3p; BAX; Parkinson's disease model (PD model); neuronal damage
资金
- Public Welfare Project of Zhejiang Science and Technology Department [2017C37150, 2017C33114]
- Zhejiang Medical Science and Technology General Project [2018KY033]
The study elucidated the relationship and mechanism of SNHG1 and miR-216a-3p in Parkinson's disease (PD), revealing their regulatory roles in cell activity and apoptosis. BAX plays a crucial role in this regulatory network.
Background: Parkinson's disease (PD) is a common central nervous system degenerative disease in middle-aged and elderly people. Our study aimed to illuminate the relationship and mechanism of long-chain non-coding RNA SNHG1 and miRNA (miR)-216a-3p in PD. Methods: Human neuroblastoma cell lines were treated with MPP+ to construct a PD model. Real-time fluorescent quantitative PCR was used to detect the cellular expression of SNHG1. Neuronal cell activity and apoptosis were compared before and after SNHG1 knock-down, as was neuronal miR-216a-3p expression. Further, a luciferase reporter gene experiment was performed to verify BAX as the target of miR-216a-3p. Anti-miR-216a-3p and BAX were co-transfected into PD model cells, and neuronal cellular activity and apoptosis were observed. Finally, the potential regulatory network of SNHG1/miR-216a-3p/BAX in PD was investigated. Results: The expression of miR-216a-3p was decreased in the PD model cells, and re-expression reversed the high apoptotic rate and cell vitality inhibition in PD model cells. SNHG1 interacted with miR-216a-3p and negatively regulated its upstream molecules, while miR-216a-3p attenuated the effect of SNHG1 knockdown on neurons. The overexpression of BAX in the PD cell model blocked the damage by miR-216a-3p to neurons. At the same time, SNHG1 acted as a coordinator, mediating the regulation of BAX via miR-216a-3p, thereby affecting the activity and apoptotic rate of neurons in the PD model. Conclusions: SNHG1 interacts with miR-216a-3p to regulate the expression of BAX. This SNHG1/miR-216a-3p/BAX molecular regulatory network is implicated in the pathogenesis of PD.
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