PubMed 23434582
Referenced in: none
Automatically associated channels: Nav1.7
Title: Endothelin-1-induced down-regulation of NaV1.7 expression in adrenal chromaffin cells: attenuation of catecholamine secretion and tau dephosphorylation.
Authors: Takayuki Nemoto, Toshihiko Yanagita, Toyoaki Maruta, Chihiro Sugita, Shinya Satoh, Tasuku Kanai, Akihiko Wada, Manabu Murakami
Journal, date & volume: FEBS Lett., 2013 Apr 2 , 587, 898-905
PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/23434582
Abstract
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 NaV1.7 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 NaV1.7. Our results indicated that endothelin-1 decreased the protein level of NaV1.7 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 NaV1.7 diminishes NaV1.7-related catecholamine secretion and dephosphorylation of tau.