Gene expression profiles and related immune-inflammatory factors in the cerebral arteries in mouse models of subarachnoid haemorrhage

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.