Abstract
Intracerebral hemorrhage (ICH) represents the most lethal form of stroke. We sought to identify potential genes that might contribute to progression of hypertension-induced spontaneous ICH (HIS-ICH). RNA-sequencing data set of cerebral vessel samples from HIS-ICH mice and normal mice was obtained from the Gene Expression Omnibus. Differential expression genes in HIS-ICH samples were obtained compared with normal samples followed by functional enrichment analysis. What is more, we explored the potential gene coexpression module (GCM) for HIS-ICH progression by using weighted gene coexpression network analysis. We further conducted protein–protein interaction network analysis for genes contained in GCM that was closely correlated with HIS-ICH to disclose their biological interactions. As a result, 554 genes were found to aberrantly express in HIS-ICH mice compared with normal mice, which were mainly associated with cancer-related pathways in addition to some well-known ICH-related pathways. A total of 28 GCMs were obtained, and darkturquoise module that contained 85 genes, which were closely associated with mitochondrion and hydrolase activity, was significantly correlated with HIS-ICH progression. Besides, we identified dense biological interactions among some genes in darkturquoise, such as Psma gene family and Hsp90a gene family. This study should shed new light on HIS-ICH progression and its treatment.
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