Increased Expression of TNF Receptor-Associated Factor 6 After Rat Traumatic Brain Injury

Abstract

TRAF6 (TNF receptor-associated factor 6), a member of tumor necrosis factor receptor-associated factors family was identified as a molecule that binds to the cytoplasmic domain of CD40. TRAF6 functions as an adaptor, positively regulating the NF-κB, JNK pathway. Additionally, some studies have reported that TRAF6 is required for apoptosis within the developing CNS and regulates cell fate decisions by inducing caspase 8-dependent apoptosis. However, its distribution and function in the central nervous system (CNS) lesion are not well understood. In this study, we performed an acute traumatic brain injury model in adult rats. And we mainly examined protein expression and cellular localization of TRAF6 during rat traumatic brain injury (TBI). Western blot analysis showed TRAF6 level significantly improved at 7 days after injury, and then declined during the following days. The protein expression of TRAF6 was further analysed by immunohistochemistry. In comparison to contralateral cerebral cortex, we observed a highly significant accumulation of TRAF6 at the ipsilateral brain. Immunofluorescence double-labeling showed that TRAF6 was co-expressed with NeuN and GFAP. Besides, co-localization of TRAF6/active caspase 3 and TRAF6/proliferating cell nuclear antigen (PCNA) were detected in NeuN and GFAP, respectively. We also examined the expression profiles of proliferating cell nuclear antigen (PCNA) and active caspase 3 whose changes were correlated with the expression profiles of TRAF6. In conclusion, this is the first description of TRAF6 expression in traumatic brains. Our data suggested that TRAF6 might play important roles in CNS pathophysiology after TBI.

<i>Withania somnifera</i> Extract Protects Model Neurons from In Vitro Traumatic Injury

“…No difference in c-Jun protein expression was observed between any of the groups (data not shown). Similarly, we observed no difference in protein expression of TRAF6, which is known to increase following head injury in vivo 40 (data not shown). To determine whether treatment altered apoptotic signaling, we monitored some key signaling pathways using the phospho-apoptosis antibody array from Full Moon Biosciences encompassing 247 proteins (Fig.…”

The expression changes of Numblike in rat brain cortex after traumatic brain injury

“…TRAF6 was associated with neuronal apoptpsis in the developing CNS (Lomaga et al 2000). And it has been reported TRAF6 was up-regulated after TBI in the rat brain cortex (Chen et al 2011). In the present investigations, the temporal pattern of the expression of Numbl is essentially paralleled with the expression of TFAF6 in brain cortex after TBI.…”

Increased expression of transcription initiation factor IIB after rat traumatic brain injury

“…It is generally accepted that the overall pathology of TBI often associate with apoptosis of neurons (Clark et al 1999;Keane et al 2001). Meanwhile, the apoptosis of neurons surrounding the wound after TBI had been reported (Jia et al 2010;Chen et al 2011;Shi et al 2011). However, the secondary mechanisms of delayed post-traumatic neuronal cell death are still poorly understood.…”