Calcineurin Aβ gene knockdown inhibits transient outward potassium current ion channel remodeling in hypertrophic ventricular myocyte

It has been shown that the activation of calcineurin is involved in regulating ion channel remodeling in hypertrophic cardiomyocytes. But the precise role of calcineurin in the regulation of transient outward potassium current (I to), an ion channel associated with fatal arrhythmia, r...

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Autores principales:	Yang Long, Deng Na, He Jionghong, Xia Guiling, Yang Ying, Zhao Yidong, Huo Zhaomei, Guo Chuxian
Formato:	article
Lenguaje:	EN
Publicado:	De Gruyter 2021
Materias:	ventricular hypertrophy transient outward potassium current calcineurin ion channel remodeling action potential Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/0f5f8c37c1c9456399e913db5e09b707
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spelling	oai:doaj.org-article:0f5f8c37c1c9456399e913db5e09b7072021-12-05T14:10:41ZCalcineurin Aβ gene knockdown inhibits transient outward potassium current ion channel remodeling in hypertrophic ventricular myocyte2391-541210.1515/biol-2021-0107https://doaj.org/article/0f5f8c37c1c9456399e913db5e09b7072021-09-01T00:00:00Zhttps://doi.org/10.1515/biol-2021-0107https://doaj.org/toc/2391-5412It has been shown that the activation of calcineurin is involved in regulating ion channel remodeling in hypertrophic cardiomyocytes. But the precise role of calcineurin in the regulation of transient outward potassium current (I to), an ion channel associated with fatal arrhythmia, remains controversial. This study aimed to examine the effects of calcineurin Aβ (CnAβ) gene knockdown on I to channel remodeling and action potential duration (APD) in the hypertrophic ventricular myocytes of neonatal rats. Results showed that phenylephrine stimulation caused hypertrophy of ventricular myocytes, upregulation of CnAβ protein expression, downregulation of Kv4.2 mRNA and protein expression, a decrease in I to current density, and prolongation of APD. CnAβ gene knockdown significantly inhibited the effects of phenylephrine stimulation. Our data indicate that CnAβ gene knockdown can inhibit I to channel remodeling and APD prolongation in hypertrophic neonatal rat ventricular myocytes. This finding suggests that calcineurin may be a potential target for the prevention of malignant ventricular arrhythmia in a hypertrophic heart.Yang LongDeng NaHe JionghongXia GuilingYang YingZhao YidongHuo ZhaomeiGuo ChuxianDe Gruyterarticleventricular hypertrophytransient outward potassium currentcalcineurinion channel remodelingaction potentialBiology (General)QH301-705.5ENOpen Life Sciences, Vol 16, Iss 1, Pp 1010-1021 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	ventricular hypertrophy transient outward potassium current calcineurin ion channel remodeling action potential Biology (General) QH301-705.5
spellingShingle	ventricular hypertrophy transient outward potassium current calcineurin ion channel remodeling action potential Biology (General) QH301-705.5 Yang Long Deng Na He Jionghong Xia Guiling Yang Ying Zhao Yidong Huo Zhaomei Guo Chuxian Calcineurin Aβ gene knockdown inhibits transient outward potassium current ion channel remodeling in hypertrophic ventricular myocyte
description	It has been shown that the activation of calcineurin is involved in regulating ion channel remodeling in hypertrophic cardiomyocytes. But the precise role of calcineurin in the regulation of transient outward potassium current (I to), an ion channel associated with fatal arrhythmia, remains controversial. This study aimed to examine the effects of calcineurin Aβ (CnAβ) gene knockdown on I to channel remodeling and action potential duration (APD) in the hypertrophic ventricular myocytes of neonatal rats. Results showed that phenylephrine stimulation caused hypertrophy of ventricular myocytes, upregulation of CnAβ protein expression, downregulation of Kv4.2 mRNA and protein expression, a decrease in I to current density, and prolongation of APD. CnAβ gene knockdown significantly inhibited the effects of phenylephrine stimulation. Our data indicate that CnAβ gene knockdown can inhibit I to channel remodeling and APD prolongation in hypertrophic neonatal rat ventricular myocytes. This finding suggests that calcineurin may be a potential target for the prevention of malignant ventricular arrhythmia in a hypertrophic heart.
format	article
author	Yang Long Deng Na He Jionghong Xia Guiling Yang Ying Zhao Yidong Huo Zhaomei Guo Chuxian
author_facet	Yang Long Deng Na He Jionghong Xia Guiling Yang Ying Zhao Yidong Huo Zhaomei Guo Chuxian
author_sort	Yang Long
title	Calcineurin Aβ gene knockdown inhibits transient outward potassium current ion channel remodeling in hypertrophic ventricular myocyte
title_short	Calcineurin Aβ gene knockdown inhibits transient outward potassium current ion channel remodeling in hypertrophic ventricular myocyte
title_full	Calcineurin Aβ gene knockdown inhibits transient outward potassium current ion channel remodeling in hypertrophic ventricular myocyte
title_fullStr	Calcineurin Aβ gene knockdown inhibits transient outward potassium current ion channel remodeling in hypertrophic ventricular myocyte
title_full_unstemmed	Calcineurin Aβ gene knockdown inhibits transient outward potassium current ion channel remodeling in hypertrophic ventricular myocyte
title_sort	calcineurin aβ gene knockdown inhibits transient outward potassium current ion channel remodeling in hypertrophic ventricular myocyte
publisher	De Gruyter
publishDate	2021
url	https://doaj.org/article/0f5f8c37c1c9456399e913db5e09b707
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Calcineurin Aβ gene knockdown inhibits transient outward potassium current ion channel remodeling in hypertrophic ventricular myocyte

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