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Updated: Aug 16, 2026
Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury
Published on: September 4, 2013
The biphasic function of microglia in ischemic stroke
Yuanyuan Ma1, Jixian Wang2, Yongting Wang3
1Department of Neurology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, China; Neuroscience and Neuroengineering Research Center, Med-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China.
Abstract:
Microglia are brain resident macrophages originated from primitive progenitor cells in the yolk sac. Microglia can be activated within hours and recruited to the lesion site. Traditionally, microglia activation is considered to play a deleterious role in ischemic stroke, as inhibition of microglia activation attenuates ischemia induced brain injury. However, increasing evidence show that microglia activation is critical for attenuating neuronal apoptosis, enhancing neurogenesis, and promoting functional recovery after cerebral ischemia. Differential polarization of microglia could likely explain the biphasic role of microglia in ischemia. We comprehensively reviewed the mechanisms involved in regulating microglia activation and polarization. The latest discoveries of microRNAs in modulating microglia function are discussed. In addition, the interaction between microglia and other cells including neurons, astrocytes, oligodendrocytes, and stem cells were also reviewed. Future therapies targeting microglia may not exclusively aim at suppressing microglia activation, but also at modulating microglia polarization at different stages of ischemic stroke. More work is needed to elucidate the cellular and molecular mechanisms of microglia polarization under ischemic environment. The roles of microRNAs and transplanted stem cells in mediating microglia activation and polarization during brain ischemia also need to be further studied.
Insights
Microglia, the brain's immune cells, have a dual role in ischemic stroke, both harming and healing. Therapies should focus on modulating their behavior, not just suppressing activation, for better recovery.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Microglia are the primary immune cells of the central nervous system, originating from primitive progenitor cells in the yolk sac.
- Traditionally, microglia activation post-ischemic stroke was considered detrimental, but emerging evidence highlights their beneficial roles in neuroprotection and recovery.
- The complex and often opposing functions of microglia suggest a biphasic role, potentially explained by differential polarization.
Purpose of the Study:
- To comprehensively review the mechanisms regulating microglia activation and polarization in the context of ischemic stroke.
- To discuss the role of microRNAs in modulating microglia function during brain ischemia.
- To examine the interactions between microglia and other brain cells (neurons, astrocytes, oligodendrocytes, stem cells) in ischemic stroke.
Main Methods:
- Literature review and synthesis of existing research on microglia biology and ischemic stroke.
- Analysis of studies investigating microglia activation, polarization, and their functional outcomes.
- Examination of molecular mechanisms, including microRNAs, and cell-cell interactions.
Main Results:
- Microglia activation exhibits a biphasic role in ischemic stroke, contributing to both injury and repair.
- Differential polarization of microglia is a key factor influencing their pro-inflammatory or anti-inflammatory responses.
- MicroRNAs and interactions with other brain cells significantly modulate microglia behavior during ischemia.
Conclusions:
- Future therapeutic strategies for ischemic stroke should aim to modulate microglia polarization rather than solely suppressing activation.
- Further research is crucial to fully understand the cellular and molecular mechanisms of microglia polarization in the ischemic brain.
- The roles of microRNAs and stem cells in mediating microglia responses during brain ischemia warrant deeper investigation.
