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

Overview

Journal Cell Mol Neurobiol

Publisher Springer

Specialties Cell Biology
Molecular Biology
Neurology

Date 2010 Nov 13

PMID 21072581

Citations 20

Authors

Jian Chen

Xiujie Wu

Bai Shao

Wei Zhao

Wei Shi

Shuangwei Zhang

Lanchun Ni

Aiguo Shen

Affiliations

Soon will be listed here.

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.

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