Up-Regulation of CCT8 Related to Neuronal Apoptosis after Traumatic Brain Injury in Adult Rats.
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.
Department of Neurosurgery, Dongtai People Affiliated Hospital of Nantong University, Yancheng, 224200, Jiangsu Province, People's Republic of China.
Xiaohong
X
Wu
Haiyan
H
Zhang
Dongjian
D
Chen
Yan
Y
Song
Rong
R
Qian
Chen
C
Chen
Xingxing
X
Mao
Xinlei
X
Chen
Weidong
W
Zhang
Bai
B
Shao
Jianhong
J
Shen
Yaohua
Y
Yan
Xinmin
X
Wu
Yonghua
Y
Liu
D000818:Animals; D017209:Apoptosis; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology; D018833:Chaperonins / Q000378:metabolism*; D007150:Immunohistochemistry; D008297:Male; D009474:Neurons / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015854:Up-Regulation
D018833:Chaperonins