ArticleCNS neuroscience & therapeutics2022
Protective role of TLR9-induced macrophage/microglia phagocytosis after experimental intracerebral hemorrhage in mice.
Article in CNS neuroscience & therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Failed resolution of inflammation in intracerebral haemorrhage.Nature reviews. Neurology · 2026Review
- SLC27A3-dependent lipid metabolic reprogramming by trilobatin suppresses microglial mtDNA/TLR9-driven inflammatory activation in traumatic brain injury.Journal of neuroinflammation · 2026Article
- Toll-like receptor 9 promotes aortic chondrogenesis and calcification in apolipoprotein E-deficient mice.Heart and vessels · 2026Article
- Mechanisms and Clinical Significance of Endosomal Toll-Like Receptors in Neurological Diseases.Molecular neurobiology · 2025Review
- Atorvastatin Protects Against the Macrophage/Microglia-Related Neuroinflammation via Inhibiting Lipocalin-2 in Mouse Experimental Intracerebral Hemorrhage Model.Cellular and molecular neurobiology · 2025Article
- Preliminary Analysis of Aging-Related Genes in Intracerebral Hemorrhage by Integration of Bulk and Single-Cell RNA Sequencing Technology.International journal of general medicine · 2024Article
- Inflammatory changes in the choroid plexus following subarachnoid hemorrhage: the role of innate immune receptors and inflammatory molecules.Frontiers in cellular neuroscience · 2024Article
- Research progress of endogenous hematoma absorption after intracerebral hemorrhage.Frontiers in neurology · 2023Review
- Higher fasting blood glucose was associated with worse in-hospital clinical outcomes in patients with primary intracerebral hemorrhage: From a large-scale nationwide longitudinal registry.CNS neuroscience & therapeutics · 2022Article
- Protective role of TLR9-induced macrophage/microglia phagocytosis after experimental intracerebral hemorrhage in mice.CNS neuroscience & therapeutics · 2022Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionIntracerebral hemorrhage (ICH) causes devastating morbidity and mortality, and studies have shown that the toxic components of hematomas play key roles in brain damage after ICH. Recent studies have found that TLR9 participates in regulating the phagocytosis of peripheral macrophages. The current study examined the role of TLR9 in macrophage/microglial (M/M) function after ICH.
methodsRAW264.7 (macrophage), BV2 (microglia), and HT22# (neurons) cell lines were transfected with lentivirus for TLR9 overexpression. Whole blood from C57BL/6 or EGFP
resultsOverexpression of TLR9 facilitated M/M phagocytosis and protected neurons from blood-derived hazards in vitro. Furthermore, ODN1826 boosted M/M activation and phagocytic function, facilitated hematoma/iron resolution, reduced brain injury, and improved neurological function recovery in ICH mice, which were abolished by clodronate injection. The experimental results indicated that the Nrf2/CD204 pathway participated in TLR9-induced M/M phagocytosis after ICH.
conclusionOur study suggests a protective role for TLR9-enhanced M/M phagocytosis via the Nrf2/CD204 pathway after ICH. Our findings may serve as potential targets for ICH treatment.
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