ArticleJournal of neuroscience research2026
Knockdown of CLEC7A Alleviates Ischemic Brain Injury by an Anti-Inflammatory Microglial Phenotype via the CXCL1/CXCR2 Axis.
Article in Journal of neuroscience research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Microglial polarization critically influences neuroinflammation and recovery after ischemic stroke. The role of C-type lectin domain family 7 member A (CLEC7A), a potential regulator in this process, remains unclear. Integrated bioinformatics analysis of Gene Expression Omnibus datasets identified CLEC7A as a hub gene. Its functional role was investigated using in vitro oxygen-glucose deprivation (OGD) models in BV2 microglia/HT22 neuron co-cultures and in vivo rat middle cerebral artery occlusion (MCAO) models. CLEC7A was knocked down in vitro and in vivo. Functional outcomes were assessed via infarct volume and neurobehavioral scores. Levels of inflammation factors were evaluated by enzyme-linked immunosorbent assay, and microglial polarization markers were assessed by western blot, immunohistochemistry, and immunofluorescence. Recombinant Chemokine (C-X-C motif) ligand 1 (CXCL1) agonist was employed for rescue experiments. Herein, CLEC7A knockdown reduced MCAO-induced infarct size, attenuated brain injury, and neurological deficits in vivo, and improved cell viability and reduced apoptosis in vitro. Furthermore, CLEC7A knockdown suppressed pro-inflammatory microglial phenotypic markers while enhancing anti-inflammatory markers in vivo and in vitro. This protective effect was mediated through the Cytokine-cytokine receptor interaction pathway, specifically via downregulation of CXCL1/C-X-C motif chemokine receptor 2 (CXCR2), as the benefits were reversed by recombinant CXCL1 treatment. In summary, silencing CLEC7A alleviates ischemic brain injury by promoting an anti-inflammatory microglial phenotype. Targeting CLEC7A to inhibit the CXCL1/CXCR2 axis represents a promising therapeutic strategy for mitigating neuroinflammation and improving recovery after stroke.
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