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Esophageal Cancer-Related Gene-4 Contributes to Lipopolysaccharide-Induced Ion Channel Dysfunction in hiPSC-Derived Cardiomyocytes

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资源类型：
Pubmed体系：
作者：
Xu Qiang[1,2] * ; Zhang Xiangjie[3] * ; Hao Maolin[3] * ; Dang Xitong[3] ; Xu QianQian[3] ; Cyganek Lukas[4,5] ; Akin Ibrahim[2,6] ; Tang Dan[7] ; Liao Bin[8] ; Zhou Xiaobo[2,3,6,*2] ; Lan Huan[3,*1] ;
机构： [1]School of Basic Medical Science, Southwest Medical University, Luzhou, People’s Republic of China [2]First Department of Medicine, Faculty ofMedicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Mannheim, Germany [3]Key Laboratory of Medical Electrophysiology,Ministry of Education & Medical Electrophysiological Key Laboratory of Sichuan Province, Institute of Cardiovascular Research, Department ofCardiology, The Affiliated Hospital, Southwest Medical University, Luzhou, People’s Republic of China [4]Stem Cell Unit, Clinic for Cardiology andPneumology, University Medical Center Göttingen, Göttingen, Germany [5]DZHK (German Center for Cardiovascular Research), Partner Site,Göttingen, Germany [6]DZHK (German Center for Cardiovascular Research), Partner Site, Heidelberg, Mannheim, Germany [7]The First People’sHospital of Longquanyi District, Chengdu/West China Longquan Hospital, Sichuan University, Chengdu, People’s Republic of China [8]Department ofCardiac Macrovascular Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, People’s Republic of China
出处：
DOI： 10.2147/JIR.S470828
ISSN：

关键词： esophageal cancer-related gene-4 arrhythmias lipopolysaccharide human-induced pluripotent stem cell-derived cardiomyocytes inflammation

摘要：
Esophageal cancer-related gene-4 (ECRG4) participate in inflammation process and can interact with the innate immunity complex TLR4-MD2-CD14 on human granulocytes. In addition, ECRG4 participate in modulation of ion channel function and electrical activity of cardiomyocytes. However, the exact mechanism is unknown. This study aimed to test our hypothesis that ECRG4 contributes to inflammation-induced ion channel dysfunctions in cardiomyocytes.Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) generated from three donors were treated with lipopolysaccharide (LPS) to establish an endotoxin-induced inflammatory model. Immunostaining, real-time PCR, and patch-clamp techniques were used for the study.ECRG4 was detected in hiPSC-CMs at different differentiation time. LPS treatment increased ECRG4 expression in hiPSC-CMs. Knockdown of ECRG4 decreased the expression level of Toll-Like-Receptor 4 (TLR4, a LPS receptor) and its associated genes and inflammatory cytokines. Furthermore, ECRG4 knockdown shortened the action potential duration (APD) and intercepted LPS-induced APD prolongation by enhancing ISK (small conductance calcium-activated K channel current) and attenuating INCX (Na/Ca exchanger current). Overexpression of ECRG4 mimicked LPS effects on ISK and INCX, which could be prevented by NFκB signaling blockers.This study demonstrated that LPS effects on cardiac ion channel function were mediated by the upregulation of ECRG4, which affects NFκB signaling. Our findings support the roles of ECRG4 in inflammatory responses and the ion channel dysfunctions induced by LPS challenge.© 2024 Xu et al.

基金：
This study was supported by the Sichuan Science and Technology Program (2022YFS0610), High-end talent attraction project of Luzhou Science & Technology Office (2024WGR203), DZHK (German Center for Cardiovascular Research) and the BMBF (German Ministry of Education and Research) (81Z0500204), Open fund of Key Laboratory of Precision Medicine to Pediatric Diseases of Shaanxi Province.
语种：
外文
PubmedID：
中科院(CAS)分区：
出版当年[2024]版：
无
最新[2023]版：
大类 | 2 区 医学
小类 | 3 区 免疫学
第一作者：
第一作者机构： [1]School of Basic Medical Science, Southwest Medical University, Luzhou, People’s Republic of China [2]First Department of Medicine, Faculty ofMedicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Mannheim, Germany
共同第一作者：
通讯作者：
通讯机构： [2]First Department of Medicine, Faculty ofMedicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Mannheim, Germany [3]Key Laboratory of Medical Electrophysiology,Ministry of Education & Medical Electrophysiological Key Laboratory of Sichuan Province, Institute of Cardiovascular Research, Department ofCardiology, The Affiliated Hospital, Southwest Medical University, Luzhou, People’s Republic of China [6]DZHK (German Center for Cardiovascular Research), Partner Site, Heidelberg, Mannheim, Germany [*1]Key Laboratory of Medical Electrophysiology, Ministry of Education & Medical Electrophysiological Key Laboratory of Sichuan Province, Institute of Cardiovascular Research, No. 1 section 1 of Xiang Lin Road, Longmatan District, Luzhou City, Sichuan, People’s Republic of China [*2]First Department of Medicine, Faculty of Medicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Theodor-Kutzer-Ufer 1-3, Mannheim, Baden-Württemberg, Germany
推荐引用方式(GB/T 7714)：
Xu Qiang,Zhang Xiangjie,Hao Maolin,et al.Esophageal Cancer-Related Gene-4 Contributes to Lipopolysaccharide-Induced Ion Channel Dysfunction in hiPSC-Derived Cardiomyocytes[J].Journal Of Inflammation Research.2024,17:10183-10197.doi:10.2147/JIR.S470828.
APA：
Xu Qiang,Zhang Xiangjie,Hao Maolin,Dang Xitong,Xu QianQian...&Lan Huan.(2024).Esophageal Cancer-Related Gene-4 Contributes to Lipopolysaccharide-Induced Ion Channel Dysfunction in hiPSC-Derived Cardiomyocytes.Journal Of Inflammation Research,17,
MLA：
Xu Qiang,et al."Esophageal Cancer-Related Gene-4 Contributes to Lipopolysaccharide-Induced Ion Channel Dysfunction in hiPSC-Derived Cardiomyocytes".Journal Of Inflammation Research 17.(2024):10183-10197

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