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IL7R depletion mitigates neuroinflammation and ischemic stroke via AKT dephosphorylation dependent LCP1 suppression in mice

ABSTRACT: Stroke remains a leading cause of death and long-term disability worldwide. After reperfusion following ischemic stroke, peripheral immune cells infiltrate the injured brain hemisphere and exacerbate secondary damage. Among these cells, monocytes are among the predominant population. In this study, we performed single-cell RNA sequencing of immune cells isolated from the brain 72 h after infarction and characterized the heterogeneity of brain infiltrating monocyte-derived macrophages. We identified an IL7R+ macrophage subset with high fatty-acid metabolism scores 3 days after ischemic stroke in mice. In vitro oxygen glucose deprivation cell model, Il7r expression was significantly increased, accompanied by upregulation of the PI3K-AKT pathway. IL7R knockdown decreased phosphorylated Akt and LCP1 levels, and LCP1 knockdown further reduced arachidonic acid, a key mediator of proinflammatory protein translation, as revealed by bulk RNA-seq and metabolomics analyses. Consistent with these in vitro results, IL7R depleted mice exhibited smaller infarct volumes and improved neurological function. Collectively, our findings provide mechanistic insight into how IL7R–pAKT-LCP1 signaling shapes immune-cell metabolism during stroke-induced neuroinflammation and suggest potential therapeutic opportunities targeting immunometabolic pathways in ischemic stroke.

ORGANISM(S): Mus musculus

PROVIDER: GSE313981 | GEO | 2026/07/29

REPOSITORIES: GEO

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Project description:Background: Previous study showed that stroke may be a potential first sign of neoplasia. But the relationship between them remains unclear. Besides, ischemic stroke is a complex brain disease, which involves cell death or complex immune regulation. Thus, it is necessary to reveal the association of tumor immune microenvironment and cell death with ischemic stroke. Methods: Here, a photothrombosis-induced ischemic injury models of brain and skull was established. We compared and analyzed the pattern of gene expression profile between brain and skull after ischemic injury by transcriptome analysis. Further, we investigated the enrichment of relevant differential genes in cancer pathways and cell death pathways, and analyzed changes in the immune microenvironment after ischemic injury. Moreover, the pan-cancer genomic and prognosis analysis of ischemic injury related gene set were performed. Results: The results showed that the gene expression patterns were different in temporal and spatial locations after ischemic injury. We found that the effect on the transcriptome of the brain after skull ischemic injury was particularly large, but it could be recovered in a short period, while the effect on the skull after brain ischemic injury was long-lasting. The expression of genes related to ischemic injury is also associated with cell death and cancer hallmark pathways. In addition, changes in the abundance of immune cells indicate that brain ischemic injury may disrupt its immune microenvironment for a longer time, while skull can better balance the stability of immune microenvironment. Moreover, the brain ischemic injury-related gene sets are highly correlated with a variety of tumors, especially GBM, KIRC, LGG and UVM after stroke have a greater risk of death. Conclusion: This study gives us a new understanding of the role of the skull in brain ischemic injury, and reveals the association of tumor immune microenvironment and cell death with ischemic stroke.

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IL7R depletion mitigates neuroinflammation and ischemic stroke via AKT dephosphorylation dependent LCP1 suppression in mice

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