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Brain-infiltrating ILC2s-derived alpha-calcitonin gene-related peptide promoting angiogenic sprouting accelerates post-stroke angiogenesis

ABSTRACT: Group 2 innate lymphoid cells (ILC2s) are key players in immune regulation and tissue repair in barrier immunity, but they are rarely seen in the brain. Since ILC2s can be intrinsically expanded by IL2/IL2 antibody complex, we investigated the transcriptomic changes induced by IL2/IL2 antibody complex (IL2-JES6-1) after ischemic stroke, we performed single-cell RNA sequencing of the CD45high immune cells from the infarcted hemisphere at day 14 after MCAO using 10x Genomics scRNAseq. To investigate the key mechanism of ILC2s-mediated long-term recovery after ischemic stroke, we performed single-cell RNA sequencing of the infarcted hemisphere at day 14 after MCAO using 10x Genomics scRNAseq.

ORGANISM(S): Mus musculus

PROVIDER: GSE303092 | GEO | 2025/07/23

REPOSITORIES: GEO

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Project description:Astrogliosis is a hallmark of the response to brain ischemia, comprised of changes in gene expression and morphology. Hsp72 protects from cerebral ischemia, and although several mechanisms of protection have been investigated, effects on astrocyte activation are unknown. To identify potential mechanisms of protection, gene expression was assessed in mice subjected to middle cerebral artery (MCAO) or sham surgery, of either wildtype (WT) or Hsp72-overexpressing (Hsp72Tg) mice. After stroke, both genotypes exhibited genes related to cell death, stress response, and immune response. Furthermore, genes indicative of astrocyte activation, including cytoskeletal proteins and cytokines, were upregulated. To measure astrocyte activation after stroke, detailed histological and morphological analyses were performed in the cortical penumbra after stroke using unbiased stereology. Consistent with other reports, we observed a marked and persistent increase in glial fibrillary acidic protein (GFAP ) as soon as 3 hours after MCAO. In contrast, vimentin immunoreactivity appeared 12-24 hours after stroke, peaked at 72 hours, and returned to baseline after 30 days. Surprisingly, no change in overall astrocyte number was observed based on glutamine synthetase (GS) immunoreactivity. To determine if Hsp72Tg mice exhibited altered astrocyte activation compared to WT controls, morphological evaluation by fractal analysis was used. Overexpression of Hsp72 reduced astrocyte cell area, arbor area, and to a lesser extent fractal dimension, 72 hours following stroke. In conclusion, in vivo overexpression of Hsp72 alters gene expression following stroke, including genes involved in astrocyte activation, and decreases astrocyte activation acutely following MCAO. Thus, modulation of astrogliosis may be a neuroprotective mechanism exerted by Hsp72 after ischemia. A total of 10 samples were analyzed, with 5 of each genotype, wildtype (WT) and Hsp72-overexpressing (Hsp72Tg) mice. Of the 5 in each group, 3 received middle cerebral artery occlusion (MCAO) and 2 received a sham surgery. The sham samples serve as the controls for the MCAO samples in each genotype. All samples were taken from the ischemic or control hemisphere 24 hours after surgery.

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Brain-infiltrating ILC2s-derived alpha-calcitonin gene-related peptide promoting angiogenic sprouting accelerates post-stroke angiogenesis

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