Abstract
BACKGROUND: Spinal cord injury (SCI) is highly related to the devastating sensory and motor dysfunction. METHODS: The GSE45006 gene expression profile dataset was downloaded from Gene Expression Omnibus, which was collected from 24 rats including 20 animals with injured T7 spinal cords using an aneurysm clip impact-compression injury model and killed after 1 day, 3 days, 1 week, 2 weeks, and 8 weeks and four sham-operated rats. Differentially expressed genes (DEGs) between the injured rats at each time point and the sham-operated rats were screened. DEGs commonly detected throughout different time points were further identified, followed by comparing the expression level of these DEGs at each time point between the injured spinal cord samples and controls. Pathway enrichment analysis of the common DEGs was performed. RESULTS: The difference in the expression level of 416 common DEGs was significant between the injured spinal cord samples and the controls at each time point (P < 0.05), with the most significant difference 1 day after SCI. The common DEGs were enriched in three pathways, namely Fcγ R-mediated phagocytosis, mitogen-activated protein kinase (MAPK) signaling pathway, and chemokine signaling pathway. AKT3 and RAC2 were enriched in all the three pathways; RAP1B in both MAPK signaling pathway and chemokine signaling pathway; and VAV1, LYN, and HCK in both Fcγ R-mediated phagocytosis and chemokine signaling pathway. CONCLUSIONS: This study has confirmed the occurrence of neuronal death, inflammation, and neuronal regeneration after SCI. AKT3, RAC2, VAV1, RAP18, LYN, and HCK may have critical roles in the pathological responses to SCI.