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Updated: Mar 18, 2026

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease
Published on: October 3, 2012
miR-124 regulates cell apoptosis and autophagy in dopaminergic neurons and protects them by regulating AMPK/mTOR
Xin Gong1, Huiqing Wang2, Yongyi Ye2
1Department of Neurosurgery, Zhujiang Hospital, Southern Medical University; The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China, Guangdong Provincial Key Laboratory on Brain Function Repair and RegenerationGuangzhou 510282, Guangdong, China; Department of Neurosurgery, Hunan Provincial People's HospitalChangsha 410005, Hunan, China.
Abstract:
The important roles of miR-124 in the development and progression of various diseases are being increasing recognized. This study was aimed to investigate the potential roles of miR-124 in dopaminergic (DA) neuronal apoptosis and autophagy in Parkinson's disease (PD) and to explore their mechanisms. Human SH-SY5Y cells that are treated with MPTP were transfected with mature miR-124 vector and control empty vector. The effect of MPTP on miR-124 mRNA level was analyzed using RT-PCR analysis. Furthermore, the effects of miR-124 expression on neuronal apoptosis and autophagy, as well as the expression of proteins in the AMPK/mTOR pathway, were analyzed using RT-PCR and western blotting. This study found that miR-124 was down-regulated in the MPTP-treated (100 μM) neurons, and miR-124 suppression significantly increased cell apoptosis and induced autophagy-associated protein expression, including that of Beclin 1 and increased the ratio of LC3 II/LC3 I compared with that in controls. In addition, in vitro rescue of miR-124 significantly decreased the percentage of apoptotic cells and the ratio of LC3 II/LC3 I, findings that were approximately equal to the controls. Moreover, miR-124 suppression increased p-AMPK but decreased p-mTOR levels in neurons. Our study suggested that miR-124 functions as a protector of DA neurons during PD through the involvement of cell apoptosis and autophagy by regulating the AMPK/mTOR pathway.
Insights
MicroRNA-124 (miR-124) protects dopaminergic neurons in Parkinson's disease (PD) by regulating apoptosis and autophagy. Its suppression increases neuronal death and alters autophagy, while restoration offers protection via the AMPK/mTOR pathway.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- MicroRNA-124 (miR-124) is increasingly recognized for its roles in disease development.
- Parkinson's disease (PD) involves dopaminergic (DA) neuronal loss, apoptosis, and altered autophagy.
- Understanding miR-124's function in PD pathogenesis is crucial.
Purpose of the Study:
- To investigate the role of miR-124 in DA neuronal apoptosis and autophagy in PD.
- To explore the underlying molecular mechanisms involving the AMPK/mTOR pathway.
Main Methods:
- MPTP-treated human SH-SY5Y cells were used as a PD model.
- RT-PCR and western blotting analyzed miR-124 mRNA, apoptosis, autophagy markers (Beclin 1, LC3 II/LC3 I), and AMPK/mTOR pathway proteins.
- miR-124 levels were manipulated using vector transfection.
Main Results:
- MPTP treatment downregulated miR-124 in neurons.
- miR-124 suppression increased DA neuronal apoptosis and induced autophagy.
- Restoring miR-124 decreased apoptosis and normalized autophagy markers.
- miR-124 suppression altered the AMPK/mTOR pathway, increasing p-AMPK and decreasing p-mTOR.
Conclusions:
- miR-124 acts as a protective factor for DA neurons in PD.
- Its protective effects are mediated through the regulation of apoptosis and autophagy.
- The AMPK/mTOR pathway is a key mechanism through which miR-124 exerts its neuroprotective functions in PD.
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