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Characterization and Isolation of Mouse Primary Microglia by Density Gradient Centrifugation
Published on: February 16, 2018
Microglia as a unique cellular target in the treatment of stroke: potential neurotoxic mediators produced by
1CoCensys Inc., Irvine, CA 92718, USA.
Abstract:
The sequalae evoked by an initial ischemic event in the CNS are incredibly complex and involve a wide range of short-term and long-term metabolic adaptations. With regard to the 'penumbra' area, in which cell death occurs over a 1 to 3 day period, defining the roles of potential neurotoxic mediators is crucial. In this regard, upon cellular activation after an ischemic episode, microglia, the resident macrophages of the CNS, can produce large quantities of a number of neurotoxic mediators. These factors include excitatory amino acids, proteases, cytokinases and nitric oxides. In this manuscript, these mediators are reviewed with regard to the potential utility of suppression of microglial function, via immunosuppressive agents, in the treatment of stroke.
Insights
Central nervous system (CNS) stroke triggers complex metabolic changes. Suppressing microglial function may offer a novel therapeutic strategy for stroke by reducing neurotoxic mediators.
Area of Science:
- Neuroscience
- Immunology
- Pathophysiology
Background:
- Ischemic stroke in the central nervous system (CNS) induces complex metabolic adaptations.
- The penumbra region is characterized by cell death over 1–3 days, necessitating identification of neurotoxic mediators.
- Microglia, the CNS resident macrophages, become activated post-ischemia and release neurotoxic factors.
Purpose of the Study:
- To review neurotoxic mediators released by activated microglia following CNS ischemic events.
- To explore the potential of suppressing microglial function as a therapeutic approach for stroke treatment.
Main Methods:
- Literature review of microglial activation and neurotoxic mediator production post-stroke.
- Analysis of the role of excitatory amino acids, proteases, cytokines, and nitric oxides.
- Evaluation of immunosuppressive agents for mitigating microglial function.
Main Results:
- Activated microglia produce significant quantities of neurotoxic mediators, including excitatory amino acids, proteases, cytokines, and nitric oxides.
- These mediators contribute to the complex sequelae of ischemic events in the CNS.
- Microglial function suppression presents a potential therapeutic avenue.
Conclusions:
- Microglial activation and subsequent release of neurotoxic mediators play a critical role in stroke pathophysiology.
- Targeting microglial function with immunosuppressive agents may be a viable strategy for stroke treatment.
