To explore the key genes, core cell subsets, and cell communication mechanisms underlying neural injury repair after intracerebral hemorrhage.

The rat intracerebral hemorrhage transcriptome dataset GSE288102, mouse intracerebral hemorrhage microglia transcriptome dataset GSE266602, and mouse intracerebral hemorrhage brain tissue single-cell RNA sequencing dataset GSE167593 were downloaded from the GEO database. The limma package was used to screen differentially expressed genes (DEGs), and the intersection of DEGs from the two transcriptome datasets was obtained to identify common DEGs. GO and KEGG enrichment analyses were performed using the DAVID database, and a protein-protein interaction (PPI) network was constructed via the STRING database. Key genes were screened using Cytoscape. Quality control, dimensionality reduction, clustering, and cell annotation of single-cell data were completed with the Seurat package, and intercellular communication pathways were analyzed using CellChat.

A total of 96 common DEGs were identified. GO terms was mainly enriched in immune cell activation, leukocyte activation, and injury repair-related processes, while KEGG enrichment was found in the ECM-receptor interaction pathway and the PI3K-Akt signaling pathway. Ten hub genes were screened, including LGALS3, ITGB2, TLR2, TIMP1, FN1, CD44, ICAM1, CCL2, TGFB1, and ITGAM. Single-cell RNA analysis identified five core cell populations: neurons, oligodendrocytes, oligodendrocyte precursor cells, microglia, and astrocytes. The hub genes showed specific expression in each cell subset: LGALS3 was downregulated and TGFB1 was upregulated in neurons; TGFB1, CCL2, and ICAM1 were significantly upregulated in astrocytes; and FN1 and TGFB1 were upregulated in microglia. Cell communication analysis revealed that SPP1- (ITGA5+ITGB1) and SPP1- (ITGAV+ITGB1) were the core signaling pathways for neural repair after intracerebral hemorrhage.

This study identified 10 core genes, 5 key cell populations, and 2 core cell communication pathways involved in neural injury repair after intracerebral hemorrhage, providing a reliable basis for investigating the mechanisms of neural repair and screening potential therapeutic targets for intracerebral hemorrhage.