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Chloride channel conductance is required for NGF-induced neurite outgrowth in PC12 cells

Cited 7 time in Web of Science Cited 7 time in Scopus
Authors
Kim, Soo Yeon; Shin, Dong Hun; Kim, Sung Joon; Park, Joobae; Bae, Chang-Dae; Koo, Byung-Soo; Jeon, Songhee
Issue Date
2010-04
Publisher
PERGAMON-ELSEVIER SCIENCE LTD
Citation
NEUROCHEMISTRY INTERNATIONAL; Vol.56 5; 663-669
Keywords
Chloride channelTrkA receptorNGFPC12 cellsNeurite outgrowth
Abstract
We have previously shown that in PC12 cells: (1) high extracellular KCl induces moesin phosphorylation, an event which was dependent on chloride channel activation, and (2) NGF induces moesin phosphorylation which is required for neurite outgrowth. These results suggest that NGF-induced intracellular signaling and neurite outgrowth is also mediated by activation of anion channels. Using a patch-clamp technique, we found that NGF treatment increased anionic conductance in PC12 cells, an effect which was completely blocked by NPPB, a chloride channel inhibitor. Also, the NGF-induced moesin phosphorylation was suppressed by NPPB. Additionally, NPPB and SITS, another chloride channel blocker, suppressed NGF-induced TrkA phosphorylation and subsequent PI3K/Akt phosphorylation and Rac1 activation in PC12 cells. Moreover, the chloride channel inhibitors also suppressed the neurite outgrowth and decreased the cell viability in response to long-term treatment of NGF. In summary, our results suggest that chloride ion flux plays an important role in TrkA-mediated signaling pathway during NGF-induced differentiation of PC12 cells. (C) 2010 Elsevier Ltd. All rights reserved.
ISSN
0197-0186
Language
English
URI
http://hdl.handle.net/10371/76228
DOI
https://doi.org/10.1016/j.neuint.2010.01.015
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Physiology (생리학교실)Journal Papers (저널논문_생리학교실)
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