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MEF2D Participates in Microglia-Mediated Neuroprotection in Cerebral Ischemia-Reperfusion Rats
Likai Shi1, Baowei Li1, Guoqing Chen1
1Department of Anesthesiology, The First Medical Center of the Chinese People's Liberation Army (PLA) General Hospital, No. 28 Fuxing Road, Beijing, China.
Objective:
Microglial activation is a vital process in the neuroinflammatory response induced by I/R injury. It has been reported that myocyte enhancer factor (MEF)2D expression in activated microglia is associated with microglia-induced inflammatory responses and plays an important role in neuronal survival. This research aimed to investigate the role and mechanism of MEF2D in microglial activation and neuroinflammation in cerebral I/R in vitro and in vivo.
Methods:
A cerebral I/R model was established. In vitro, neuronal, or microglial cells were exposed to oxygen-glucose deprivation and reoxygenation to mimic I/R. MEF2D overexpression was induced, and siRNA was administered in vitro and in vivo. Microglial polarization; MEF2D, nuclear transcription factor (NF)-κb, TLR4, and cytokine levels; neuronal injury; mitochondrial function; brain injury and cognitive function were detected in the different groups in vitro and in vivo.
Results:
We found that oxygen-glucose deprivation increased MEF2D expression in a time-dependent manner in BV2 cells and primary microglia. MEF2D overexpression inhibited microglial activation, the expression of NF-κb and TLR, cytokine levels, and neuronal injury in microglia exposed to oxygen-glucose deprivation and reoxygenation. In the middle cerebral artery occlusion model, microglial activation, the neuroinflammatory response, mitochondrial dysfunction, brain injury, and cognitive function were improved by MEF2D overexpression and aggravated by MEF2D siRNA treatment.
Conclusion:
These results indicate that MEF2D is a necessary molecule for neuroinflammation regulation and neuronal injury in cerebral ischemia.
Insights
Myocyte enhancer factor (MEF)2D protects neurons by regulating microglial activation and neuroinflammation following cerebral ischemia. MEF2D overexpression reduces brain injury and improves cognitive function after ischemic stroke.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Microglial activation is central to neuroinflammation after ischemic stroke.
- Myocyte enhancer factor (MEF)2D in microglia influences inflammatory responses and neuronal survival.
Purpose of the Study:
- Investigate the role and mechanism of MEF2D in microglial activation and neuroinflammation during cerebral ischemia-reperfusion (I/R) injury.
- Determine MEF2D's impact on neuronal survival and brain function in vitro and in vivo.
Main Methods:
- Established a cerebral I/R model and used oxygen-glucose deprivation/reoxygenation for in vitro studies.
- Utilized MEF2D overexpression and siRNA for manipulation in vitro and in vivo.
- Assessed microglial polarization, inflammatory markers (MEF2D, NF-κb, TLR4), cytokine levels, neuronal injury, mitochondrial function, brain damage, and cognitive function.
Main Results:
- Oxygen-glucose deprivation increased MEF2D expression in microglia.
- MEF2D overexpression suppressed microglial activation, inflammation, and neuronal injury.
- In vivo studies showed MEF2D overexpression improved brain injury and cognitive function, while siRNA worsened outcomes.
Conclusions:
- MEF2D is crucial for regulating neuroinflammation and mitigating neuronal injury in cerebral ischemia.
- Targeting MEF2D presents a potential therapeutic strategy for ischemic stroke.
