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

Chen, Jian; Wu, Xiujie; Shao, Bai; Zhao, Wei; Shi, Wei; Zhang, Shuangwei; Ni, Lei; Shen, Aiguo

doi:10.1007/s10571-010-9617-6

Cited by 33 publications

(30 citation statements)

References 26 publications

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“…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.…”

Section: Resultssupporting

confidence: 50%

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

2016

Cell Transplant

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Withania somnifera has been used in traditional medicine for a variety of neural disorders. Recently, chronic neurodegenerative conditions have been shown to benefit from treatment with this extract. To evaluate the action of this extract on traumatically injured neurons, the efficacy of W. somnifera root extract as a neuroprotective agent was examined in cultured model neurons exposed to an in vitro injury system designed to mimic mild traumatic brain injury (TBI). Neuronal health was evaluated by staining with annexin V (an early, apoptotic feature) and monitoring released lactate dehydrogenase activity (a terminal cell loss parameter). Potential mechanisms underlying the observed neuroprotection were examined. Additionally, morphological changes were monitored following injury and treatment. Although no differences were found in the expression of the antioxidant transcription factor nuclear factor erythroid 2-like 2 (Nrf2) or other Nrf2-related downstream components, significant changes were seen in apoptotic signaling. Treatment with the extract resulted in an increased length of neurites projecting from the neuronal cell body after injury. W. somnifera extract treatment also resulted in reduced cell death in the model neuron TBI system. The cell death factor Bax was involved (its expression was reduced 2-fold by the treatment) and injury-induced reduction in neurite lengths and numbers was reversed by the treatment. This all indicates that W. somnifera root extract was neuroprotective and could have therapeutic potential to target factors involved in secondary injury and longterm sequelae of mild TBI.

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Section: Resultssupporting

confidence: 50%

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

2016

Cell Transplant

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“…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.…”

Section: Discussionmentioning

confidence: 93%

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

Jiang

Yan

et al. 2012

J Mol Hist

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Numblike (Numbl) plays an important role in ependymal wall integrity and subventricular zone neuroblast survival. And Numbl is specifically expressed in the brain. However, its expression and function in the central nervous system lesion are still unclear. In this study, we performed a traumatic brain injury (TBI) model in adult rats and investigated the dynamic changes of Numbl expression in the brain cortex. Western blot and immunohistochemistry analysis revealed that Numbl was present in normal brain. It gradually decreased, reached the lowest point at day 3 after TBI, and then increased during the following days. Double immunofluorescence staining showed that Numbl immunoreactivity was found in neurons, but not astrocytes and microglia. Moreover, the 3rd day post injury was the apoptotic peak implied by the alteration of caspase-3. All these results suggested that Numbl may be involved in the pathophysiology of TBI and further research is needed to have a good understanding of its function and mechanism.

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“…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.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2011

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The protein TFIIB is a general transcription initiation factor that plays a pivotal role in the preinitiation complex (PIC) and selects the transcription initiation site. However, its distribution and function in the central nervous system (CNS) remains unclear. In the present study, we mainly investigated the expression and cellular localization of TFIIB during traumatic brain injury (TBI). Western blot analysis revealed that TFIIB was present in normal rat brain cortex. It gradually increased, reached a peak at the 5th day after TBI, and then decreased. Importantly, more TFIIB was colocalized with astrocytes and microglia, which are largely proliferated. In addition, Western blot detection showed that the 5th day post injury was also the proliferation peak indicated by the elevated expression of PCNA. Importantly, injury-induced expression of TFIIB was colabelled by proliferating cell nuclear antigen (proliferating cells marker). These data suggested that TFIIB may be implicated in the proliferation of astrocytes and microglia and the recovery of neurological outcomes. But the inherent mechanisms remained unknown. Further studies are needed to confirm the exact role of TFIIB after brain injury.

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

Cited by 33 publications

References 26 publications

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

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

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

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

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