Global ETD Search

1	Regulations of Sodium Channels by Wnt Signalling in Cardiomyocytes Chu, Cencen 23 June 2022 (has links) Background: The canonical Wnt/β-catenin pathway is activated in a variety of heart diseases, such as myocardial infarction and cardiac hypertrophy, that are associated with altered ion channel expressions and increased risk of cardiac arrhythmias. Previous work from our lab has demonstrated that the Wnt/β-catenin signalling (Wnt signalling) inhibits sodium (Na+) current in rat cardiomyocytes. In this project, we aim to investigate the mechanisms that underlie the inhibition of Na+ current by Wnt signalling in both rat and human cardiomyocytes. Results: In both neonatal rat ventricular myocytes (NRVMs) and human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs), activation of the Wnt/β-catenin signalling led to reduced level of Na+ channel gene transcript (Scn5a), channel protein (Nav1.5) and channel current density. This suggests that reduced Scn5a expression is likely the primary mechanism for reduced Na+ current. In addition, we found that activation of the Wnt/β-catenin signalling in both NRVMs and iPSC-CMs upregulated Tbx3 transcript and protein levels, which is a transcription factor that is known to suppress Scn5a transcription. In NRVMs, siRNA-mediated Tbx3 knockdown attenuated (by ~30%) Wnt-induced reductions in Scn5a and Nav1.5 levels. Conclusions: Our findings are consistent with the conclusion that Wnt/β-catenin signalling inhibits Na+ current in both rat and human cardiomyocytes by reducing Scn5a levels, with Tbx3 as one of the mediators. Tbx3 Wnt signalling Cardiomyocyte Cardiac sodium channel Scn5a
2	Modelling genetic heart diseases with patient-specific induced pluripotent stem cells Stauske, Michael 18 June 2014 (has links) No description available. 570 induced pluripotent stem cells disease modelling Brugada syndrome cardiac sodium channel Biologie (PPN619462639)
3	Cardiac sodium channel mutation associated with epinephrine-induced QT prolongation and sinus node dysfunction / エピネフリン誘発性QT延長及び洞結節機能不全に関連する心筋ナトリウムチャネル遺伝子変異の解析 Jiarong, Chen 23 March 2016 (has links) 京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第19609号 / 医博第4116号 / 新制\|\|医\|\|1015(附属図書館) / 32645 / 京都大学大学院医学研究科医学専攻 / (主査)教授岩井一宏, 教授小杉眞司, 教授瀬原淳子 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM SCN5A epinephrine long-QT syndrome adrenergic stimulation cardiac sodium channel mutation 490
4	Gain-of-function mutations in SCN5A gene lead to type-3 long QT syndrome Fang, Fang 04 December 2012 (has links) No description available. Biology Chemistry Genetics Health Sciences Arrhythmia LQTS Cardiac sodium channel SCN5A Late sodium current Calcium overload Calcium handling Calcium transient
5	NaV1.5 Modulation: From Ionic Channels to Cardiac Conduction and Substrate Heterogeneity Raad, Nour 16 January 2014 (has links) No description available. 571.4 Antiarrhythmic drugs Optical Mapping Action potential duration Spatial dispersion of repolarization Cardiac depolarization Conduction velocity Anisotropy Duchenne muscular dystrophy mdx - mouse model Dystrophin ΔKPQ mouse model Long QT Syndrome 3 Cardiac Sodium Channel (NaV1.5) Flecainide Maximum upstroke velocity Least Squares Ellipsis Fitting Method Area Fitting Method Plane Fitting Method Conduction abnormalities Voltage sensitive dyes Cardiac arrhythmia Functional heterogeneity Spatial-temporal heterogeneity Proarrhythmia Activation maps Symmetry breaking Intrinsic cardiac heterogeneity Biologie (PPN619462639)

1

Page generated in 0.0759 seconds