Abstract
The interferon regulatory factor (IRF) family was first discovered as a set of transcriptional regulators of the type I interferon system in 1988. In mammals, the IRF family includes nine members that play important roles in the immune system, oncogenesis, and apoptosis. However, the distribution and the function of IRF6 in the central nervous system are limited. In this study, we established an adult rat traumatic brain injury (TBI) model. Compared to the sham brain cortex, Western blot and immunohistochemistry showed significant upregulation of IRF6 in the ipsilateral brain cortex after TBI. Immunofluorescence double-labeling showed that IRF6 completely co-localized with neurons, not astrocytes or oligodendrocytes. Furthermore, we detected that the neuronal apoptosis marker active caspase-3 co-localized with IRF6 in neurons. Additionally, IRF6 knockdown in PC12 cells in vitro resulted in a decrease in active caspase-3 expression and an increase in Bcl-2 and p-Akt expression. We conclude that IRF6 might promote neuronal apoptosis by inhibiting Akt phosphorylation after TBI.