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Endothelin‐1‐induced down‐regulation of Na V 1.7 expression in adrenal chromaffin cells: Attenuation of catecholamine secretion and tau dephosphorylation
Author(s) -
Nemoto Takayuki,
Yanagita Toshihiko,
Maruta Toyoaki,
Sugita Chihiro,
Satoh Shinya,
Kanai Tasuku,
Wada Akihiko,
Murakami Manabu
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.02.013
Subject(s) - catecholamine , dephosphorylation , secretion , endocrinology , medicine , chemistry , endothelin 1 , chromaffin cell , adrenal medulla , phosphorylation , biology , biochemistry , receptor , phosphatase
Endothelin‐1 and voltage‐dependent sodium channels are involved in control and suppression of neuropathological factors, which contribute to sculpting the neuronal network. We previously demonstrated that veratridine‐induced Na V 1.7 sodium channel activation caused intracellular calcium elevation, catecholamine secretion and tau dephosphorylation in adrenal chromaffin cells. The aim of this study was to examine whether endothelin‐1 could modulate Na V 1.7. Our results indicated that endothelin‐1 decreased the protein level of Na V 1.7 and the veratridine‐induced increase in intracellular calcium. In addition, it also abolished the veratridine‐induced dephosphorylation of tau and the phosphorylation of glycogen synthase kinase‐3β and extracellular signal‐regulated kinase. These findings suggest that the endothelin‐1‐induced down‐regulation of Na V 1.7 diminishes Na V 1.7‐related catecholamine secretion and dephosphorylation of tau.