Abstract The study aimed to identify key genes involved in cerebral vasospasm (CVS) after subarachnoid haemorrhage (SAH). GSE46696 of basilar arteries of SAH mice and normal controls were downloaded from the Gene Expression Omnibus (GEO). Integrated microarray analysis was performed to identify differentially expressed genes (DEGs). GO and KEGG pathway enrichment analyses of DEGs were performed with ClueGO. The protein–protein interaction (PPI) networks were constructed using Cytoscape software. A total of 4103 DEGs were identified; among them, 254 DEGs (63 up-regulated genes and 191 down-regulated genes) showed significant differences at p < 0.05. GO analysis showed that the identified DEGs were over-represented in 16 GO terms. KEGG pathway analysis showed that pathways in immune inflammation were significantly enriched pathways for DEGs. DEGs with relatively frequent interactions after CVS secondary to SAH included MIKI, Cmpk2, TIr3, Psmb9, Ddx58, Lgals9, Ifi44, Stat2, Rsad2, Oas2, Usp18, H28, Irf7 and als3bp. Multiple genes were involved in the regulation of the immune response in the pathogenesis of SAH, including Ripk3, Ifih1, IL10, Reg3g, SIc11a1, NF-κB, Tlr7, Parp9, Rab7b, Dhx58, Gpx2, Zbp1, Aim2, Rsad2, Lgals9, TLR4, Adar, Zc3hav1, KIrk1, Irf7, IL-1β, Trafd1, Ddx58 and Trim5. Our findings revealed the gene expression profiles of the cerebral arteries in SAH mouse models, and speculated that DHx58 gene plays an important role in the immune response through regulating inflammatory cytokines expression, which may be a potential target in the treatment of CVS after SAH. Our finding provided new clues for understanding the mechanism of SAH.

中文翻译：

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蛛网膜下腔出血小鼠模型脑动脉基因表达谱及相关免疫炎症因子

摘要 本研究旨在确定参与蛛网膜下腔出血（SAH）后脑血管痉挛（CVS）的关键基因。SAH 小鼠和正常对照的基底动脉 GSE46696 从基因表达综合 (GEO) 下载。进行集成微阵列分析以鉴定差异表达基因（DEG）。使用 ClueGO 对 DEG 进行 GO 和 KEGG 通路富集分析。使用 Cytoscape 软件构建蛋白质 - 蛋白质相互作用（PPI）网络。共鉴定出 4103 个 DEG；其中，254个DEGs（63个上调基因和191个下调基因）在p < 0.05时表现出显着差异。GO 分析表明，已识别的 DEG 在 16 个 GO 术语中过多。KEGG通路分析表明，免疫炎症通路是DEGs的显着富集通路。继发于 SAH 的 CVS 后相互作用相对频繁的 DEG 包括 MIKI、Cmpk2、TIr3、Psmb9、Ddx58、Lgals9、Ifi44、Stat2、Rsad2、Oas2、Usp18、H28、Irf7 和 als3bp。在SAH的发病机制中，多个基因参与免疫反应的调控，包括Ripk3、Ifih1、IL10、Reg3g、SIc11a1、NF-κB、Tlr7、Parp9、Rab7b、Dhx58、Gpx2、Zbp1、Aim2、Rsad2、Lgals9、 TLR4、Adar、Zc3hav1、KIrk1、Irf7、IL-1β、Trafd1、Ddx58 和 Trim5。我们的研究结果揭示了 SAH 小鼠模型脑动脉的基因表达谱，并推测 DHx58 基因通过调节炎症细胞因子的表达在免疫反应中发挥重要作用，这可能是 SAH 后 CVS 治疗的潜在靶点。我们的发现为理解SAH的机制提供了新的线索。