ArticleTranslational stroke research2021
Inhibition of Dectin-1 Ameliorates Neuroinflammation by Regulating Microglia/Macrophage Phenotype After Intracerebral Hemorrhage in Mice.
Article in Translational stroke research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 59 citations in OpenAlex.
- Orally activatable membrane fusion-mitochondria hitchhiking on intestinal macrophages for targeted therapy of bacterial meningitis and neuroinflammation.Bioactive materials · 2027Article
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- Synthetic Ligands of Myeloid C-Type Lectin Receptors.Chembiochem : a European journal of chemical biology · 2026Review
- Laminarin attenuates neuroinflammation in MPTP-induced Parkinson's disease mouse model via inhibiting dectin-1/Syk/NF-κB signaling.Inflammopharmacology · 2026Article
- Ginsenoside Rg2 attenuates secondary brain injury following intracerebral hemorrhage by inhibiting NLRP3-mediated pyroptosis.Journal of neuroinflammation · 2026Article
- Red Blood Cell-Derived Exosomes Deliver Complement C5 to Exacerbate Neuroinflammation and Neuronal Injury after Intracerebral Hemorrhage.Inflammation · 2026Article
- Quercetin inhibits microglial pyroptosis following intracerebral hemorrhage via the TLR2/MyD88/NF-κB signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Targeting the interactions between neutrophils and microglia: a novel strategy for anti-inflammatory treatment of stroke.Acta pharmacologica Sinica · 2026Review
- Clec7a Drives Microglial Activation-Mediated Myelin Degradation in Sepsis-Associated Encephalopathy.Inflammation · 2026Article
- Microglial dectin-1/Frontiers in immunology · 2026Article
- Targeting the Dectin-1 Receptor in Neuroinflammation: Therapeutic Implications for Neuropsychiatric Disorders.ACS chemical neuroscience · 2025Review
- Unveiling the inflammatory messengers after intracerebral hemorrhage: the crosstalk between peripheral NETs and microglia.Frontiers in immunology · 2025Review
- Microglial Mechanisms and Therapeutic Potential in Brain Injury Post-Intracerebral Hemorrhage.Journal of inflammation research · 2025Review
- Emerging roles for ITAM and ITIM receptor signaling in microglial biology and Alzheimer's disease-related amyloidosis.Journal of neurochemistry · 2024Review
- Knockout of Dectin-1 does not modify disease onset or progression in a MATR3 S85C knock-in mouse model of ALS.Heliyon · 2024Article
- Astrocyte-Derived Extracellular Vesicular miR-143-3p Dampens Autophagic Degradation of Endothelial Adhesion Molecules and Promotes Neutrophil Transendothelial Migration after Acute Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Human platelet lysate: a potential therapeutic for intracerebral hemorrhage.Frontiers in neuroscience · 2024Review
- Spi1 regulates the microglial/macrophage inflammatory response via the PI3K/AKT/mTOR signaling pathway after intracerebral hemorrhage.Neural regeneration research · 2024Article
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Corrections and comments
- Erratum issued
Authors and funding
15 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polarization of microglia/macrophages toward the pro-inflammatory phenotype is an important contributor to neuroinflammation after intracerebral hemorrhage (ICH). Dectin-1 is a pattern recognition receptor that has been reported to play a key role in regulating neuroinflammation in ischemic stroke and spinal cord injury. However, the role and mechanism of action of Dectin-1 after ICH remains unclear. In this study, we investigated the effect of Dectin-1 on modulating the microglia/macrophage phenotype and neuroinflammation and the possible underlying mechanism after ICH. We found that Dectin-1 expression increased after ICH, and was mainly localized in microglia/macrophages. Neutrophil infiltration and microglia/macrophage polarization toward the pro-inflammatory phenotype increased after ICH. However, treatment with a Dectin-1 inhibitor reversed these phenomena and induced a shift the anti-inflammatory phenotype in microglia/macrophages; this resulted in alleviation of neurological dysfunction and facilitated hematoma clearance after ICH. We also found that Dectin-1 crosstalks with the downstream pro-inflammatory pathway, Card9/NF-κB, by activating spleen tyrosine kinase (Syk) both in vivo and in vitro. In conclusion, our data suggest that Dectin-1 is involved in the microglia/macrophage polarization and functional recovery after ICH, and that this mechanism, at least in part, may contribute to the involvement of the Syk/Card9/NF-kB pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.