Nitric oxide down-regulates voltage-gated Na+ channel in cardiomyocytes possibly through S-nitrosylation-mediated signaling

Abstract Nitric oxide (NO) is produced from endothelial cells and cardiomyocytes composing the myocardium and benefits cardiac function through both vascular-dependent and—independent effects. This study was purposed to investigate the possible adverse effect of NO focusing on the voltage-gated Na+...

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Autores principales:	Pu Wang, Mengyan Wei, Xiufang Zhu, Yangong Liu, Kenshi Yoshimura, Mingqi Zheng, Gang Liu, Shinichiro Kume, Masaki Morishima, Tatsuki Kurokawa, Katsushige Ono
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/0a296701e62e480999648e0b93287942
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spelling	oai:doaj.org-article:0a296701e62e480999648e0b932879422021-12-02T15:00:39ZNitric oxide down-regulates voltage-gated Na+ channel in cardiomyocytes possibly through S-nitrosylation-mediated signaling10.1038/s41598-021-90840-02045-2322https://doaj.org/article/0a296701e62e480999648e0b932879422021-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-90840-0https://doaj.org/toc/2045-2322Abstract Nitric oxide (NO) is produced from endothelial cells and cardiomyocytes composing the myocardium and benefits cardiac function through both vascular-dependent and—independent effects. This study was purposed to investigate the possible adverse effect of NO focusing on the voltage-gated Na+ channel in cardiomyocytes. We carried out patch-clamp experiments on rat neonatal cardiomyocytes demonstrating that NOC-18, an NO donor, significantly reduced Na+ channel current in a dose-dependent manner by a long-term application for 24 h, accompanied by a reduction of Nav1.5-mRNA and the protein, and an increase of a transcription factor forkhead box protein O1 (FOXO1) in the nucleus. The effect of NOC-18 on the Na+ channel was blocked by an inhibitor of thiol oxidation N-ethylmaleimide, a disulfide reducing agent disulfide 1,4-Dithioerythritol, or a FOXO1 activator paclitaxel, suggesting that NO is a negative regulator of the voltage-gated Na+ channel through thiols in regulatory protein(s) for the channel transcription.Pu WangMengyan WeiXiufang ZhuYangong LiuKenshi YoshimuraMingqi ZhengGang LiuShinichiro KumeMasaki MorishimaTatsuki KurokawaKatsushige OnoNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Pu Wang Mengyan Wei Xiufang Zhu Yangong Liu Kenshi Yoshimura Mingqi Zheng Gang Liu Shinichiro Kume Masaki Morishima Tatsuki Kurokawa Katsushige Ono Nitric oxide down-regulates voltage-gated Na+ channel in cardiomyocytes possibly through S-nitrosylation-mediated signaling
description	Abstract Nitric oxide (NO) is produced from endothelial cells and cardiomyocytes composing the myocardium and benefits cardiac function through both vascular-dependent and—independent effects. This study was purposed to investigate the possible adverse effect of NO focusing on the voltage-gated Na+ channel in cardiomyocytes. We carried out patch-clamp experiments on rat neonatal cardiomyocytes demonstrating that NOC-18, an NO donor, significantly reduced Na+ channel current in a dose-dependent manner by a long-term application for 24 h, accompanied by a reduction of Nav1.5-mRNA and the protein, and an increase of a transcription factor forkhead box protein O1 (FOXO1) in the nucleus. The effect of NOC-18 on the Na+ channel was blocked by an inhibitor of thiol oxidation N-ethylmaleimide, a disulfide reducing agent disulfide 1,4-Dithioerythritol, or a FOXO1 activator paclitaxel, suggesting that NO is a negative regulator of the voltage-gated Na+ channel through thiols in regulatory protein(s) for the channel transcription.
format	article
author	Pu Wang Mengyan Wei Xiufang Zhu Yangong Liu Kenshi Yoshimura Mingqi Zheng Gang Liu Shinichiro Kume Masaki Morishima Tatsuki Kurokawa Katsushige Ono
author_facet	Pu Wang Mengyan Wei Xiufang Zhu Yangong Liu Kenshi Yoshimura Mingqi Zheng Gang Liu Shinichiro Kume Masaki Morishima Tatsuki Kurokawa Katsushige Ono
author_sort	Pu Wang
title	Nitric oxide down-regulates voltage-gated Na+ channel in cardiomyocytes possibly through S-nitrosylation-mediated signaling
title_short	Nitric oxide down-regulates voltage-gated Na+ channel in cardiomyocytes possibly through S-nitrosylation-mediated signaling
title_full	Nitric oxide down-regulates voltage-gated Na+ channel in cardiomyocytes possibly through S-nitrosylation-mediated signaling
title_fullStr	Nitric oxide down-regulates voltage-gated Na+ channel in cardiomyocytes possibly through S-nitrosylation-mediated signaling
title_full_unstemmed	Nitric oxide down-regulates voltage-gated Na+ channel in cardiomyocytes possibly through S-nitrosylation-mediated signaling
title_sort	nitric oxide down-regulates voltage-gated na+ channel in cardiomyocytes possibly through s-nitrosylation-mediated signaling
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/0a296701e62e480999648e0b93287942
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Nitric oxide down-regulates voltage-gated Na+ channel in cardiomyocytes possibly through S-nitrosylation-mediated signaling

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