TY  - JOUR
PY  - 2017//
TI  - Involvement of autophagy in connexin 40 reduction in the late phase of traumatic brain injury in rats
JO  - Brain research bulletin
A1  - Che, Wei
A1  - Guo, Yijun
A1  - Yang, Wenjin
A1  - Zheng, Ping
A1  - Zeng, Jinsong
A1  - Tong, Wusong
SP  - 100
EP  - 106
VL  - 131
IS  - 
N2  - Brain trauma can activate an attenuation of connexin gap junction that is implicated in neuronal injury, but the underlying cellular mechanisms remain incompletely understood. Here, we aimed to study whether autophagy, a stress-response process for recycling of intracellular proteins and organelles, is involved in the reduction of connexin 40 (Cx40) during the late phase of traumatic brain injury (TBI). In a rat model of TBI induced by controlled cortical impact (CCI), we found that Cx40 protein in the brain started to decline at post-surgery day 2 and the decrease continued for up to day 6. Such a relatively late response of Cx40 following TBI was found to be coincident with the substantial induction of neuron degeneration and autophagy, elevated autophagic vacuole numbers, and induced LC3-II and p62 levels. At day 4 post-injury, the extent of co-localization between LC3 and Cx40 was greatly enhanced, and the reduction of Cx40 was rescued by the administration of an autophagy inhibitor chloroquine. Thus, autophagy stimulated in the injured brains may act as a suppressing mechanism to decrease gap junction protein Cx40 in the late phase of TBI.<br><br>Copyright © 2017. Published by Elsevier Inc.<p />  <p>Language: en</p>
LA  - en
SN  - 0361-9230
UR  - http://dx.doi.org/10.1016/j.brainresbull.2017.03.014
ID  - ref1
ER  -