| Literature DB >> 26285900 |
Xiaohong Wu1, Haiyan Zhang, Dongjian Chen, Yan Song, Rong Qian, Chen Chen, Xingxing Mao, Xinlei Chen, Weidong Zhang, Bai Shao, Jianhong Shen, Yaohua Yan, Xinmin Wu, Yonghua Liu.
Abstract
Traumatic brain injury (TBI) initiates a series of neurochemical and signaling changes that could eventually lead to neuronal apoptosis. Recent studies indicated that mature neurons cell cycle re-enter played a crucial role in neuronal apoptosis. In this study, we identified that the chaperonin containing TCP-1, subunit 8 (CCT8), as a member of class II chaperonins, was significantly upregulated following TBI. Moreover, double immunofluorescence staining revealed that CCT8 was co-expressed with neuronal nuclei (NeuN). Besides, co-localization of CCT8/active caspase 3 was detected in NeuN. We also examined the expression profiles of active caspase 3 whose changes were correlated with the expression of CCT8. All our findings suggested that CCT8 might be involved in the pathophysiology of brain after TBI.Entities:
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Year: 2015 PMID： 26285900 DOI： 10.1007/s11064-015-1683-1
Source DB: PubMed Journal: Neurochem Res ISSN： 0364-3190 Impact factor: 3.996