Bioinformatics analysis of gene expression profiles in the rat cerebral cortex following traumatic brain injury.

BACKGROUND Traumatic brain injury (TBI) is a serious neurodisorder commonly caused by sports related events or violence. It is the leading cause of disability in people under 40. AIM In order to elucidate the molecular mechanism of the secondary injury after TBI. MATERIALS AND METHODS In this study, we downloaded gene expression profile on TBI model with sham controls for gene set enrichment analysis and pathway analysis. RESULTS At a q-value of 5%, 361 genes were up-regulated and 373 were down-regulated in samples obtained at 48 hours after TBI. Functional analyses revealed that steroid biosynthesis, cell cycle, metal ion transport, inflammation and apoptosis were significantly dysregulated during the late period after trauma. In addition, MAPK3 (mitogen-activated protein kinase 3), was identified as the hub node in the protein-protein interaction (PPI) network constructed by the differentially expressed genes (DEGs). CONCLUSIONS Further elucidation of genes and proteins in our study may reveal their potential as novel therapeutic targets.