ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2018
Inhibition of MyD88 Signaling Skews Microglia/Macrophage Polarization and Attenuates Neuronal Apoptosis in the Hippocampus After Status Epilepticus in Mice.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 75 citations in OpenAlex.
- Prophylactic self-assembled nucleic acid hydrogel targeting retinal ganglion cell cuproptosis and microglial neuroinflammation for retinal ischemia-reperfusion injury.Bioactive materials · 2026Article
- MyD88 Deficiency Protects Mice From Experimental Autoimmune Encephalomyelitis by Influencing Both Dendritic Cells and T Cells.Immunology · 2026Article
- Targeting microglial MyD88 reprograms injury-activated microglia and promotes spinal cord repair via TGF-β signaling and biomimetic nanodelivery.Theranostics · 2026Article
- Macrophage Polarization-Related Biomarkers in Epilepsy: Integrated Bioinformatics Analysis and Clinical Validation.Journal of inflammation research · 2026Article
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- IL-1β and HMGB1 in Epileptogenesis: Recent Advances and Clinical Translation.Pharmaceuticals (Basel, Switzerland) · 2025Review
- TRIB1 silencing attenuates epilepsy by restoring mitochondrial homeostasis and suppressing microglia-driven neuroinflammation via MAPK pathway inhibition.Journal of molecular histology · 2025Article
- Pathophysiology of Status Epilepticus Revisited.International journal of molecular sciences · 2025Review
- Extracellular vesicle surface engineering with integrins (ITGAL & ITGB2) to specifically target ICAM-1-expressing endothelial cells.Journal of nanobiotechnology · 2025Article
- Article
- Imperative role of adaptor proteins in macrophage toll-like receptor signaling pathways.Future science OA · 2024Review
- Ferroptosis and Pyroptosis in Epilepsy.Molecular neurobiology · 2024Review
- Aged-Related Changes in Microglia and Neurodegenerative Diseases: Exploring the Connection.Biomedicines · 2024Review
- Article
- The immune system and metabolic products in epilepsy and glioma-associated epilepsy: emerging therapeutic directions.JCI insight · 2024Review
- Immunology of Retinitis Pigmentosa and Gene Therapy-Associated Uveitis.Cold Spring Harbor perspectives in medicine · 2024Review
- Leukocyte differential gene expression prognostic value for high versus low seizure frequency in temporal lobe epilepsy.BMC neurology · 2024Article
- Microglia and infiltrating macrophages in ictogenesis and epileptogenesis.Frontiers in molecular neuroscience · 2024Review
- Melatonin regulates microglial polarization to M2 cell via RhoA/ROCK signaling pathway in epilepsy.Immunity, inflammation and disease · 2023Article
- Beneficial Effects of ProbioticInternational journal of molecular sciences · 2023Article
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4 authors at 1 institution in 1 country.
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Abstract
Inflammation is implicated in epileptogenesis. Activated microglia and macrophages (MG/MΦ) are found in the brains of patients with epilepsy-related diseases and animal models of epilepsy. It is not yet known how the MG/MΦ activation phenotype affects pathological changes in the brain after a single seizure. In this study, we had 2 main purposes: first, to characterize post-status epilepticus (SE) inflammation by tracking MG/MΦ polarization, and, second, to explore the role of an innate immune receptor adaptor protein, namely, myeloid differentiation primary response gene 88 (MyD88), in the induction of SE in a mouse model. A lithium-pilocarpine model of seizure conditions was generated in C57BL/6 mice. The intensity and distribution of MG/MΦ polarization were tracked by fluorescent immunohistochemistry and Western blotting for the polarization markers inducible nitrogen oxygenized synthase, arginase-1, CD163, and mannose receptor. We observed steadily increasing M1 MG/MΦ along with MyD88 signal upregulation after SE in the hippocampi of mice, whereas the M2 marker arginase-1 was localized mainly in astrocytes rather than in MG/MΦ. Inhibition or gene knockout of MyD88 reduced M1 MG/MΦ and gliosis although increasing M2 MG/MΦ in the hippocampi of SE mice. MyD88 inhibition also augmented glutamate transporter 1 expression and reduced N-methyl-D-aspartate receptor NR1 subunit expression in the hippocampus to protect pyramidal neurons from apoptosis. These data suggest that MG/MΦ polarization after SE impacts the pathological outcome of the hippocampus via MyD88 signaling and point to MyD88 as a potential neuroprotective target for epilepsy therapy.
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