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Abstract
Background: Traumatic brain injury (TBI) is a brain function change caused by external forces, which is one of the main causes of death and disability worldwide. The aim of this study was to identify early diagnostic markers and potential therapeutic targets for TBI.Methods: Differences between TBI and controls in GSE89866 and GSE104687 were analyzed. The two groups of differentially expressed genes (DEGs) were combined for coexpression analysis, and the modules of interest were performed using enrichment analysis. Hub genes were identified by calculating area under curve (AUC) values of module genes, PPI network analysis, and functional similarity. Finally, the difference in immune cell infiltration between TBI and control was calculated by ssGSEA.Results: A total of 4,817 DEGs were identified in GSE89866 and 1,329 DEGs in GSE104687. They were clustered into nine modules. The genes of modules 1, 4, and 7 had the most crosstalk and were identified as important modules. Enrichment analysis revealed that they were mainly associated with neurodevelopment and immune inflammation. In the PPI network constructed by genes with top 50 AUC values in module genes, we identified the top 10 genes with the greatest connectivity. Among them, down-regulated RPL27, RPS4X, RPL23A, RPS15A, and RPL7A had similar functions and were identified as hub genes. In addition, DC and Tem were significantly up-regulated and down-regulated between TBI and control, respectively.Conclusion: We found that hub genes may have a diagnostic role for TBI. Molecular dysregulation mechanisms of TBI are associated with neurological and immune inflammation. These results may provide new ideas for the diagnosis and treatment of TBI.
Highlights
Traumatic brain injury (TBI) is an important public health problem as it is one of the leading causes of death and disability in the world (Hyder et al, 2007)
Explosion and impact are the main causes of TBI, which lead to a certain degree of cerebrovascular injury, white and gray matter damage, and neuronal and/or glial cell damage (Rodriguez et al, 2018)
To identify the gene expression characteristics of TBI, we compared the differences between TBI and control in the two datasets
Summary
Traumatic brain injury (TBI) is an important public health problem as it is one of the leading causes of death and disability in the world (Hyder et al, 2007). The peak incidence of TBI occurs in youth and older life, and it will cause morbidity and mortality in young people under 45 years of age. TBI is a diverse process that involves the interaction of many pathophysiological events and processes (Povlishock and Katz, 2005). This poses a major challenge in identifying reliable and sensitive biomarkers in TBI. Traumatic brain injury (TBI) is a brain function change caused by external forces, which is one of the main causes of death and disability worldwide.
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