Citation

Che W, Guo Y, Yang W, Zheng P, Zeng J, Tong W. Brain Res. Bull. 2017; 131: 100-106.

Affiliation

The People's Hospital of Pudong New Area,490 South Chuanhuan Road, Chuansha New Town, Shanghai 201299, PR China. Electronic address: wstong3@sina.com.

Copyright

(Copyright © 2017, Elsevier Publishing)

DOI

10.1016/j.brainresbull.2017.03.014

PMID

28373150

Abstract

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.

Copyright © 2017. Published by Elsevier Inc.

Language: en

Keywords

Autophagy; Connexin; Gap junction; Neuron degeneration; Traumatic brain injury