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Gap junctions contribute to astrocytic resistance against zinc toxicity

Authors
 Jinu Lee  ;  Yeong Shin Yim  ;  Chul Hoon Kim  ;  Dong Goo Kim  ;  Suk Jin Ko 
Citation
 Brain Research Bulletin, Vol.86(5-6) : 314-318, 2011 
Journal Title
 Brain Research Bulletin 
ISSN
 0361-9230 
Issue Date
2011
Abstract
Astrocytic gap junctions have been implicated in the regulation of cell viability. High amounts of extracellular zinc, which is released during ischemia, seizure, and brain trauma, can be cytotoxic to astrocytes. We tested whether gap junction coupling between astrocytes plays an important role in modulating zinc toxicity in hippocampal astrocytes. Zinc induces cell death in a dose-dependent manner in primary cultured hippocampal astrocytes. Two gap junction inhibitors, 18β-glycyrrhetinic acid and arachidonic acid, had no effect on zinc-induced cell death in low-confluence culture, where physical separation prevents gap junctions from forming. However, these inhibitors can potentiate zinc toxicity in high-confluence astrocyte cultures. Zinc toxicity was substantially suppressed upon connexin 43 overexpression, whereas knockdown caused a significant enhancement of the toxicity in high-confluence cultures. These data suggest that gap junctions in hippocampal astrocytes provide a protective role against zinc toxicity.
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/94684
DOI
10.1016/j.brainresbull.2011.08.011
Appears in Collections:
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실)
Yonsei Authors
김동구(Kim, Dong Goo) ; 김창훈(Kim, Chang Hoon) ; 임영신(Yim, Yeong Shin)
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Full Text
http://www.sciencedirect.com/science/article/pii/S0361923011002589
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