TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes

Abstract The non-selective cation channel transient receptor potential vanilloid 1 (TRPV1) is expressed throughout the cardiovascular system. Recent evidence shows a role for TRPV1 in inflammatory processes. The role of TRPV1 for myocardial inflammation has not been established yet. Human induced pl...

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Autores principales:	Katherine Sattler, Ibrahim El-Battrawy, Lukas Cyganek, Siegfried Lang, Huan Lan, Xin Li, Zhihan Zhao, Jochen Utikal, Thomas Wieland, Martin Borggrefe, Xiaobo Zhou, Ibrahim Akin
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/a7f9a71d55e74244b426387ab24d1474
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spelling	oai:doaj.org-article:a7f9a71d55e74244b426387ab24d14742021-12-02T16:17:18ZTRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes10.1038/s41598-021-93958-32045-2322https://doaj.org/article/a7f9a71d55e74244b426387ab24d14742021-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-93958-3https://doaj.org/toc/2045-2322Abstract The non-selective cation channel transient receptor potential vanilloid 1 (TRPV1) is expressed throughout the cardiovascular system. Recent evidence shows a role for TRPV1 in inflammatory processes. The role of TRPV1 for myocardial inflammation has not been established yet. Human induced pluripotent stem cell (iPSC)-derived cardiomyocytes (hiPSC-CM) from 4 healthy donors were incubated with lipopolysaccharides (LPS, 6 h), TRPV1 agonist capsaicin (CAP, 20 min) or the antagonist capsazepine (CPZ, 20 min). TRPV1 expression was studied by PCR and western blotting. TRPV1 internalization was analyzed by immunofluorescence. Interleukin-6 (IL-6) secretion and phosphorylation of JNK, p38 and ERK were determined by ELISA. TRPV1-associated ion channel current was measured by patch clamp. TRPV1-mRNA and -protein were expressed in hiPSC-CM. TRPV1 was localized in the plasma membrane. LPS significantly increased secretion of IL-6 by 2.3-fold, which was prevented by pre-incubation with CPZ. LPS induced TRPV1 internalization. Phosphorylation levels of ERK, p38 or JNK were not altered by TRPV1 stimulation or inhibition. LPS and IL-6 significantly lowered TRPV1-mediated ion channel current. TRPV1 mediates the LPS-induced inflammation in cardiomyocytes, associated with changes of cellular electrophysiology. LPS-induced inflammation results in TRPV1 internalization. Further studies have to examine the underlying pathways and the clinical relevance of these findings.Katherine SattlerIbrahim El-BattrawyLukas CyganekSiegfried LangHuan LanXin LiZhihan ZhaoJochen UtikalThomas WielandMartin BorggrefeXiaobo ZhouIbrahim AkinNature 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 Katherine Sattler Ibrahim El-Battrawy Lukas Cyganek Siegfried Lang Huan Lan Xin Li Zhihan Zhao Jochen Utikal Thomas Wieland Martin Borggrefe Xiaobo Zhou Ibrahim Akin TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes
description	Abstract The non-selective cation channel transient receptor potential vanilloid 1 (TRPV1) is expressed throughout the cardiovascular system. Recent evidence shows a role for TRPV1 in inflammatory processes. The role of TRPV1 for myocardial inflammation has not been established yet. Human induced pluripotent stem cell (iPSC)-derived cardiomyocytes (hiPSC-CM) from 4 healthy donors were incubated with lipopolysaccharides (LPS, 6 h), TRPV1 agonist capsaicin (CAP, 20 min) or the antagonist capsazepine (CPZ, 20 min). TRPV1 expression was studied by PCR and western blotting. TRPV1 internalization was analyzed by immunofluorescence. Interleukin-6 (IL-6) secretion and phosphorylation of JNK, p38 and ERK were determined by ELISA. TRPV1-associated ion channel current was measured by patch clamp. TRPV1-mRNA and -protein were expressed in hiPSC-CM. TRPV1 was localized in the plasma membrane. LPS significantly increased secretion of IL-6 by 2.3-fold, which was prevented by pre-incubation with CPZ. LPS induced TRPV1 internalization. Phosphorylation levels of ERK, p38 or JNK were not altered by TRPV1 stimulation or inhibition. LPS and IL-6 significantly lowered TRPV1-mediated ion channel current. TRPV1 mediates the LPS-induced inflammation in cardiomyocytes, associated with changes of cellular electrophysiology. LPS-induced inflammation results in TRPV1 internalization. Further studies have to examine the underlying pathways and the clinical relevance of these findings.
format	article
author	Katherine Sattler Ibrahim El-Battrawy Lukas Cyganek Siegfried Lang Huan Lan Xin Li Zhihan Zhao Jochen Utikal Thomas Wieland Martin Borggrefe Xiaobo Zhou Ibrahim Akin
author_facet	Katherine Sattler Ibrahim El-Battrawy Lukas Cyganek Siegfried Lang Huan Lan Xin Li Zhihan Zhao Jochen Utikal Thomas Wieland Martin Borggrefe Xiaobo Zhou Ibrahim Akin
author_sort	Katherine Sattler
title	TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes
title_short	TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes
title_full	TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes
title_fullStr	TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes
title_full_unstemmed	TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes
title_sort	trpv1 activation and internalization is part of the lps-induced inflammation in human ipsc-derived cardiomyocytes
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/a7f9a71d55e74244b426387ab24d1474
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TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes

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