Calenduloside E protects against myocardial ischemia-reperfusion injury induced calcium overload by enhancing autophagy and inhibiting L-type Ca2+ channels through BAG3

Calenduloside E (CE) is a saponin isolated from Aralia elata (Miq) Seem, which has anti-cardiovascular disease effects. This study aims to evaluate the anti-myocardial ischemia-reperfusion injury (MIRI) mechanisms of CE and regulation of BAG3 on calcium overload. We adopted siRNA to interfere with B...

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Autores principales:	Ruiying Wang, Min Wang, Bo Liu, Huibo Xu, Jingxue Ye, Xiaobo Sun, Guibo Sun
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2022
Materias:	calenduloside E myocardial ischemia-reperfusion injury L-type Ca2+ channels BAG3 calcium overload autophagy Therapeutics. Pharmacology RM1-950
Acceso en línea:	https://doaj.org/article/fb63903b138c44a08284f0c48e477f8c
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spelling	oai:doaj.org-article:fb63903b138c44a08284f0c48e477f8c2021-11-18T04:43:38ZCalenduloside E protects against myocardial ischemia-reperfusion injury induced calcium overload by enhancing autophagy and inhibiting L-type Ca2+ channels through BAG30753-332210.1016/j.biopha.2021.112432https://doaj.org/article/fb63903b138c44a08284f0c48e477f8c2022-01-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S075333222101218Xhttps://doaj.org/toc/0753-3322Calenduloside E (CE) is a saponin isolated from Aralia elata (Miq) Seem, which has anti-cardiovascular disease effects. This study aims to evaluate the anti-myocardial ischemia-reperfusion injury (MIRI) mechanisms of CE and regulation of BAG3 on calcium overload. We adopted siRNA to interfere with BAG3 expression in H9c2 cardiomyocytes and used adenovirus to interfere with BAG3 expression (Ad-BAG3) in primary neonatal rat cardiomyocytes (PNRCMs) to clarify the role of BAG3 in mitigating MIRI by CE. The results showed that CE reduced calcium overload, and Ad-BAG3 had a significant regulatory effect on L-type Ca2+ channels (LTCC) but no effects on other calcium-related proteins. And BAG3 and LTCC were colocalized in myocardial tissue and BAG3 inhibited LTCC expression. Surprisingly, CE had no regulatory effect on LTCC mRNA, but CE promoted LTCC degradation through the autophagy-lysosomal pathway rather than the ubiquitination-protease pathway. Autophagy inhibitor played a negative regulation of cardiomyocyte contraction rhythm and field potential signals. Ad-BAG3 inhibited autophagy by regulating the expression of autophagy-related proteins and autophagy agonist treatment suppressed calcium overload. Therefore, CE promoted autophagy through BAG3, thereby regulating LTCC expression, inhibiting calcium overload, and ultimately reducing MIRI.Ruiying WangMin WangBo LiuHuibo XuJingxue YeXiaobo SunGuibo SunElsevierarticlecalenduloside Emyocardial ischemia-reperfusion injuryL-type Ca2+ channelsBAG3calcium overloadautophagyTherapeutics. PharmacologyRM1-950ENBiomedicine & Pharmacotherapy, Vol 145, Iss , Pp 112432- (2022)
institution	DOAJ
collection	DOAJ
language	EN
topic	calenduloside E myocardial ischemia-reperfusion injury L-type Ca2+ channels BAG3 calcium overload autophagy Therapeutics. Pharmacology RM1-950
spellingShingle	calenduloside E myocardial ischemia-reperfusion injury L-type Ca2+ channels BAG3 calcium overload autophagy Therapeutics. Pharmacology RM1-950 Ruiying Wang Min Wang Bo Liu Huibo Xu Jingxue Ye Xiaobo Sun Guibo Sun Calenduloside E protects against myocardial ischemia-reperfusion injury induced calcium overload by enhancing autophagy and inhibiting L-type Ca2+ channels through BAG3
description	Calenduloside E (CE) is a saponin isolated from Aralia elata (Miq) Seem, which has anti-cardiovascular disease effects. This study aims to evaluate the anti-myocardial ischemia-reperfusion injury (MIRI) mechanisms of CE and regulation of BAG3 on calcium overload. We adopted siRNA to interfere with BAG3 expression in H9c2 cardiomyocytes and used adenovirus to interfere with BAG3 expression (Ad-BAG3) in primary neonatal rat cardiomyocytes (PNRCMs) to clarify the role of BAG3 in mitigating MIRI by CE. The results showed that CE reduced calcium overload, and Ad-BAG3 had a significant regulatory effect on L-type Ca2+ channels (LTCC) but no effects on other calcium-related proteins. And BAG3 and LTCC were colocalized in myocardial tissue and BAG3 inhibited LTCC expression. Surprisingly, CE had no regulatory effect on LTCC mRNA, but CE promoted LTCC degradation through the autophagy-lysosomal pathway rather than the ubiquitination-protease pathway. Autophagy inhibitor played a negative regulation of cardiomyocyte contraction rhythm and field potential signals. Ad-BAG3 inhibited autophagy by regulating the expression of autophagy-related proteins and autophagy agonist treatment suppressed calcium overload. Therefore, CE promoted autophagy through BAG3, thereby regulating LTCC expression, inhibiting calcium overload, and ultimately reducing MIRI.
format	article
author	Ruiying Wang Min Wang Bo Liu Huibo Xu Jingxue Ye Xiaobo Sun Guibo Sun
author_facet	Ruiying Wang Min Wang Bo Liu Huibo Xu Jingxue Ye Xiaobo Sun Guibo Sun
author_sort	Ruiying Wang
title	Calenduloside E protects against myocardial ischemia-reperfusion injury induced calcium overload by enhancing autophagy and inhibiting L-type Ca2+ channels through BAG3
title_short	Calenduloside E protects against myocardial ischemia-reperfusion injury induced calcium overload by enhancing autophagy and inhibiting L-type Ca2+ channels through BAG3
title_full	Calenduloside E protects against myocardial ischemia-reperfusion injury induced calcium overload by enhancing autophagy and inhibiting L-type Ca2+ channels through BAG3
title_fullStr	Calenduloside E protects against myocardial ischemia-reperfusion injury induced calcium overload by enhancing autophagy and inhibiting L-type Ca2+ channels through BAG3
title_full_unstemmed	Calenduloside E protects against myocardial ischemia-reperfusion injury induced calcium overload by enhancing autophagy and inhibiting L-type Ca2+ channels through BAG3
title_sort	calenduloside e protects against myocardial ischemia-reperfusion injury induced calcium overload by enhancing autophagy and inhibiting l-type ca2+ channels through bag3
publisher	Elsevier
publishDate	2022
url	https://doaj.org/article/fb63903b138c44a08284f0c48e477f8c
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Calenduloside E protects against myocardial ischemia-reperfusion injury induced calcium overload by enhancing autophagy and inhibiting L-type Ca2+ channels through BAG3

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