Journal
MEDICAL SCIENCE MONITOR
Volume 26, Issue -, Pages -Publisher
INT SCIENTIFIC INFORMATION, INC
DOI: 10.12659/MSM.922032
Keywords
Apoptosis; Autophagy; MicroRNAs; Parkinson Disease
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Funding
- Science and Technology Plan Project of Nanjing Military Region of PLA [14MS091]
- Youth Nursery Fund of the 909th Hospital of PLA [16Y001]
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Background: Parkinson's disease (PD) is a movement disorder. microRNA (miR)-133 expression is reduced in PD patients and in mice with a dopamine neuron deficiency. We aimed to identify the mechanism of miR-133a in apoptosis and autophagy in PD. Material/Methods: The optimal concentration of MPP+ (1-methyl-4-phenylpyridinium ion) was initially determined to construct a PD cell model. Gain-of function experiments were carried out to evaluate the role of miR-133a in PD. The levels of miR-133a, RAC1 (Ras-related C3 botulinum toxin substrate 1), apoptosis-related factors, and autophagyrelated factors were detected after detection of cell proliferation, cell cycle, and apoptosis. Transmission electron microscopy was applied to observe autophagosomes, and immunofluorescence staining was performed to detect LC3 and further analyze the effect of miR-133a on autophagy in a PD cell model. Results: Low miR-133a expression was detected in a cell model of MPP+-induced PD. After overexpressing miR-133a, cell proliferation increased, and apoptosis (cleaved caspase-3 and Bax levels decreased, while Bcl2 levels increased) and autophagy was inhibited (LC3II/I and Beclin-1 levels decreased, while p62 levels increased). MiR-133a targeted RAC1. RACY upregulation attenuated the inhibitory effects of miR-133a on PC12 cell apoptosis and autophagy. Conclusions: Our data highlighted that miR-133a overexpression prevented apoptosis and autophagy in a cell model of MPP+-induced PD by inhibiting RAC1 expression.
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