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Updated: Aug 11, 2025
A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes
Published on: February 5, 2018
Microglia and astrocytes mediate synapse engulfment in a MER tyrosine kinase-dependent manner after traumatic brain
Hui Shen1, Xiao-Jing Shi1, Lin Qi1
1Med-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Abstract:
Recent studies have shown that microglia/macrophages and astrocytes can mediate synaptic phagocytosis through the MER proto-oncokinase in developmental or stroke models, but it is unclear whether the same mechanism is also active in traumatic brain injury. In this study, we established a mouse model of traumatic brain injury and found that both microglia/macrophages and astrocytes phagocytosed synapses and expression of the MER proto-oncokinase increased 14 days after injury. Specific knockout of MER in microglia/macrophages or astrocytes markedly reduced injury volume and greatly improved neurobehavioral function. In addition, in both microglia/macrophages-specific and astrocytes-specific MER knock-out mice, the number of microglia/macrophage and astrocyte phagocytosing synapses was markedly decreased, and the total number of dendritic spines was increased. Our study suggested that MER proto-oncokinase expression in microglia/macrophages and astrocytes may play an important role in synaptic phagocytosis, and inhibiting this process could be a new strategy for treating traumatic brain injury.
Insights
MER proto-oncokinase drives synaptic phagocytosis by microglia/macrophages and astrocytes after traumatic brain injury. Inhibiting this MER pathway offers a potential therapeutic strategy for brain injury recovery.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Microglia/macrophages and astrocytes mediate synaptic phagocytosis via MER proto-oncokinase in development and stroke.
- The role of MER proto-oncokinase in synaptic phagocytosis following traumatic brain injury (TBI) remains unexplored.
Purpose of the Study:
- To investigate the involvement of MER proto-oncokinase in synaptic phagocytosis in a mouse model of TBI.
- To evaluate the therapeutic potential of inhibiting MER-mediated synaptic phagocytosis for TBI treatment.
Main Methods:
- Establishment of a mouse model of traumatic brain injury.
- Analysis of MER proto-oncokinase expression in microglia/macrophages and astrocytes post-TBI.
- Generation of microglia/macrophage-specific and astrocyte-specific MER knock-out mouse lines.
- Assessment of injury volume, neurobehavioral function, synaptic phagocytosis, and dendritic spine density.
Main Results:
- Both microglia/macrophages and astrocytes phagocytosed synapses in the TBI model, with increased MER proto-oncokinase expression 14 days post-injury.
- Specific knockout of MER in microglia/macrophages or astrocytes significantly reduced TBI volume and improved neurobehavioral outcomes.
- MER knockout models showed decreased synaptic phagocytosis by these glial cells and increased dendritic spine density.
Conclusions:
- MER proto-oncokinase plays a critical role in mediating synaptic phagocytosis by microglia/macrophages and astrocytes after TBI.
- Inhibiting MER-mediated synaptic phagocytosis presents a promising novel therapeutic strategy for managing traumatic brain injury.
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