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.
journal_name
Neurochem Resjournal_title
Neurochemical researchauthors
Wu X,Zhang H,Chen D,Song Y,Qian R,Chen C,Mao X,Chen X,Zhang W,Shao B,Shen J,Yan Y,Wu X,Liu Ydoi
10.1007/s11064-015-1683-1subject
Has Abstractpub_date
2015-09-01 00:00:00pages
1882-91issue
9eissn
0364-3190issn
1573-6903journal_volume
40pub_type
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