Luyao Jiang1,#, Longsheng Fu2,#, Shaofeng Xiong2,3, Guosheng Cao4, Yanqin Mei2,3, Yaoqi Wu2, Jin Chen1,*, Yanni LV2,5,6,*
BIOCELL, Vol.49, No.9, pp. 1749-1769, 2025, DOI:10.32604/biocell.2025.068507
- 25 September 2025
Abstract Background: After ischemic stroke, neutrophils hyperactivate, increasing in number and worsening inflammation, causing neural damage. Prior scRNA-seq showed Lrg1 modulates cells subsentence to cerebral ischemia-reperfusion injury, but its mechanism in regulating neutrophil accumulation/differentiation post-injury is unclear. Methods: Lrg1 knockout impact on neutrophil accumulation was assessed via immunofluorescence and western blot. Three-dimensional reconstruction of immunofluorescent staining analyzed cell-cell interactions among neutrophils and microglia. scRNA-seq of WT and Lrg1-/- mice from GSE245386 and GSE279462 was conducted. Each group conducted oxidative phosphorylation scoring via Gene Set Enrichment Analysis (GSEA), while Metascape was employed to perform GO and KEGG enrichment… More >
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