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MiR-212 Attenuates MPP⁺-Induced Neuronal Damage by Targeting KLF4 in SH-SY5Y Cells
Yanfeng Song1, Ying Liu1, Xiaowei Chen2
1Department of Internal Medicine-Neurology, Hua Mei Branch of the Second People's Hospital of Liaocheng, Linqing, China.
Purpose:
Parkinson's disease (PD) is a common age-dependent neurodegenerative disease. MiR-212 has been demonstrated to exert protective effects in several neurological disorders. The present study aimed to investigate the role and underlying molecular mechanism of miR-212 in PD.
Materials And Methods:
1-methyl-4-phenylpyridinium (MPP+)-induced SH-SY5Y cells were applied as a PD model in vitro. RT-qPCR was used to measure the expression of miR-212 and Kruppel-like factor 4 (KLF4) mRNA. Western blot analysis was performed to detect the protein levels of KLF4, Notch1 and Jagged1. Cell viability and apoptosis were determined by the Cell Counting Kit-8 and flow cytometry, respectively. Quantitative analysis of caspase-3 activity, lactate dehydrogenase (LDH), reactive oxygen species (ROS), superoxide dismutase (SOD), tumor necrosis factor-α (TNF-α), and interleukin-1 beta (IL-1β) was conducted with corresponding ELISA kits. Dual-luciferase reporter assay was employed to evaluate the relationship between miR-212 and KLF4.
Results:
MiR-212 was downregulated in MPP⁺-induced SH-SY5Y cells. Also, miR-212 alleviated MPP⁺-induced SH-SY5Y cell damage, embodied by increased cell viability, decreased caspase-3 activity, LDH release, ROS production, TNF-α, and IL-1β expression, as well as elevated SOD levels. KLF4 was a direct target of miR-212, and miR-212 repressed KLF4 expression in a post-transcriptional manner. Moreover, miR-212-mediated protection effects were abated following KLF4 expression restoration in MPP⁺-induced SH-SY5Y cells, represented as lowered cell viability and enhanced apoptotic rate. Furthermore, Notch signaling was involved in the regulation of miR-212/KLF4 axis in MPP⁺-induced SH-SY5Y cells.
Conclusion:
miR-212 might attenuate MPP⁺-induced neuronal damage by regulating KLF4/Notch signaling pathway in SH-SY5Y cells, a promising target for PD therapy.
Insights
MicroRNA-212 (miR-212) shows protective effects against Parkinson's disease (PD) by downregulating Kruppel-like factor 4 (KLF4) and influencing the Notch signaling pathway, offering a potential therapeutic target.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Parkinson's disease (PD) is a prevalent age-related neurodegenerative disorder.
- MicroRNA-212 (miR-212) has demonstrated neuroprotective properties in various neurological conditions.
- The specific role and molecular mechanisms of miR-212 in PD pathogenesis remain to be fully elucidated.
Purpose of the Study:
- To investigate the role of miR-212 in Parkinson's disease.
- To explore the underlying molecular mechanisms of miR-212 action in a PD model.
- To determine if miR-212 can serve as a therapeutic target for PD.
Main Methods:
- Utilized 1-methyl-4-phenylpyridinium (MPP+)-induced SH-SY5Y cells as an in vitro model of PD.
- Quantified miR-212 and Kruppel-like factor 4 (KLF4) mRNA expression using RT-qPCR.
- Assessed protein levels of KLF4, Notch1, and Jagged1 via Western blot analysis.
- Evaluated cell viability, apoptosis, caspase-3 activity, LDH, ROS, SOD, TNF-α, and IL-1β using cell counting kits, flow cytometry, and ELISA.
- Investigated the miR-212 and KLF4 interaction using a dual-luciferase reporter assay.
Main Results:
- MiR-212 expression was significantly downregulated in MPP+-treated SH-SY5Y cells.
- Overexpression of miR-212 protected against MPP+-induced neuronal damage, evidenced by increased cell viability and reduced apoptosis markers.
- KLF4 was identified as a direct target of miR-212, with miR-212 inhibiting KLF4 expression post-transcriptionally.
- Restoring KLF4 expression diminished the protective effects of miR-212, indicating KLF4 mediates miR-212's action.
- The miR-212/KLF4 axis was found to involve the Notch signaling pathway in regulating neuronal damage.
Conclusions:
- MiR-212 attenuates MPP+-induced neuronal injury in SH-SY5Y cells, likely through the regulation of the KLF4/Notch signaling pathway.
- These findings suggest that miR-212 represents a promising therapeutic target for Parkinson's disease treatment.
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