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- Hua Zhao, Shi-Ting Li, Jin Zhu, Xu-Ming Hua, and Liang Wan.
- Department of Neurosurgery, Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China.
- World Neurosurg. 2019 Sep 1; 129: e16-e22.
BackgroundSubarachnoid hemorrhage (SAH) is an uncommon disease. Considering ruptured intracranial aneurysms as the main cause of this disease and only a minority of the intracranial aneurysms will rupture sooner or later, to understand the underlying pathology or a specific gene expression profile of an impending ruptured intracranial aneurysm is of great importance.MethodsThe transcriptome in peripheral blood cells of patients with SAH from ruptured aneurysm was compared with that of control patients suffering from headaches. The microarray dataset GSE36791 comprised 43 patients with SAH from ruptured aneurysms and 18 control patients. Differential expression analysis was performed with the R language packages to identify differentially expressed genes (DEGs). Gene Ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway database analysis were performed to identify significantly altered biological functions and pathways, respectively. The protein-protein interaction networks were constructed with information from the STRING database.ResultsA total of 528 DEGs were identified, of which 311 were upregulated and 217 downregulated. Clustering analysis confirmed that these genes can distinguish ruptured aneurysm SAH patients from the control patients. The DEGs were mainly enriched for immune/inflammation response and related pathways. Among the DEGs, 8 genes (ARG1, MAPK14, RPS2, SPI1, FYN, CEBPB, FLOT1, and CD4) were identified as the key regulators in the Protein-Protein Interaction network. MAPK14, CEBPB, FLOT1, and CD4 might be potential biomarkers of SAH.ConclusionThis study identified a range of DEGs SAH patients with ruptured aneurysms, which may enhance our current knowledge on this disease and may provide potential biomarkers of this disease.Copyright © 2019 Elsevier Inc. All rights reserved.
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