ArticleCNS neuroscience & therapeutics2023
Endothelial TREM-1 receptor regulates the blood-brain barrier integrity after intracerebral hemorrhage in mice via SYK/β-catenin signaling.
Article in CNS neuroscience & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 19 citations in OpenAlex.
- hUMSC-Exosomes suppress TREM1-p38 MAPK signaling via HMGB1-dependent mechanisms to reprogram microglial function and promote neuroprotection in ischemic stroke.Journal of nanobiotechnology · 2025Article
- Gut-derived macrophages link intestinal damage to brain injury after cardiac arrest through TREM1 signaling.Cellular & molecular immunology · 2025Article
- Role of triggering receptor expressed on myeloid cells 1/2 in secondary injury after cerebral hemorrhage.World journal of clinical cases · 2025Review
- Extracellular cold-inducible RNA-binding protein in CNS injury: molecular insights and therapeutic approaches.Journal of neuroinflammation · 2025Review
- TREM-1 inhibitor specificity and timing of treatment initiation can impact its therapeutic efficacy in cancer and inflammatory disease.Frontiers in oncology · 2025Article
- TREM-1 as a potential gatekeeper of neuroinflammatory responses: therapeutic validation and mechanistic insights in experimental traumatic brain injury.Frontiers in immunology · 2025Article
- TREM-1 and TREM-2 as therapeutic targets: clinical challenges and perspectives.Frontiers in immunology · 2024Article
- Unveiling the significance of TREM1/2 in hemorrhagic stroke: structure, function, and therapeutic implications.Frontiers in neurology · 2024Review
- Endothelial TREM-1 receptor regulates the blood-brain barrier integrity after intracerebral hemorrhage in mice via SYK/β-catenin signaling.CNS neuroscience & therapeutics · 2023Article
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6 authors at 2 institutions in 1 country.
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Abstract
backgroundIntracerebral hemorrhage (ICH) is a high mortality and disability stroke subtype. Destruction of the blood-brain barrier (BBB) is a crucial contributor to brain edema and neurological deficit after ICH. Triggering receptor expressed on myeloid cells 1 (TREM-1) has been reported to be expressed in endothelial cells, but its role in ICH remains unclear. This study aims to evaluate the role of TREM-1 on BBB permeability after ICH in mice.
methodsTwo hundred and forty-two CD1 mice were used in this study. The ICH model was established by collagenase injection. LP17 was administered intranasally at 2 or 8 h after ICH to inhibit TREM-1. To explore the underlying mechanism, SYK activation CRISPR was administered intracerebroventricularly with LP17, and Anti-mouse TREM-1 rat IgG2a (a specific TREM-1 agonist) was injected intracerebroventricularly with R406 (a specific SYK inhibitor) intraperitoneally. Neurobehavioral outcome, brain water content, BBB permeability, and protein expression were evaluated.
resultsThe expression level of the TREM-1 receptor increased rapidly as early as 6 h after ICH, and it was mainly expressed on the endotheliocytes in the neurovascular unit. Early and delayed administration of LP17 significantly decreased brain edema and improved neurobehavioral outcomes at 24 h after ICH. LP17 reduced the BBB permeability by increasing β-catenin, claudin-5 and ZO-1 expression. Furthermore, SYK activation CRISPR abolished the beneficial effect of LP17 on the expression of the above junction molecules. Meanwhile, R406 reversed the impact of the TREM-1 activator on the downregulation of β-catenin, claudin-5 and ZO-1 expression.
conclusionsThis study demonstrated that TREM-1 deteriorated BBB permeability via modulating the expression of interendothelial junction molecules after ICH, and this regulation is partly mediated by the SYK/β-catenin signaling pathway.
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