TNF receptor associated factor 3 (
TRAF3), a member of the TRAF family of
intracellular signaling proteins, can directly influence the phosphorylation status and activation of
c-Jun N-terminal kinase, participating in CD40-induced apoptosis in
carcinoma. However, its expression profile and function are still unclear in
spinal cord injury (SCI). In this study, we performed an acute
spinal cord contusion injury model in adult rats and detected the dynamic change patterns of
TRAF3 expression in spinal cord. Western blot and immunohistochemistry revealed a striking upregulation of
TRAF3 after SCI. Double immunofluorescence staining prompted that
TRAF3 immunoreactivity was found in neurons rather than astrocytes. Moreover, co-localization of
TRAF3/active
caspase-3 was detected in neuronal nuclei. To further investigate the function of
TRAF3, a neuronal cell line PC12 was employed to establish an apoptosis model in vitro. We analyzed the association of
TRAF3 with active
caspase-3 on PC12 cells by western blot and immunofluorescent labeling, which was parallel with the data in vivo. Additionally, knocking
TRAF3 down with
siRNA demonstrated the probable pro-apoptotic role of
TRAF3 in the process of neuronal apoptosis. To summarize, we firstly uncover the temporal and spatial expression changes of
TRAF3 in SCI. Our data suggest that
TRAF3 might be implicated in central nervous system pathophysiology after SCI.