EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #05020_C
长期维持人类psc来源的心肌细胞的培养基
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总览
STEMdiff™ 心肌细胞维持试剂盒可用于长期维持人多能干细胞（PSC）衍生的心肌细胞，维持时间可达一个月或更长。该试剂盒能够保持PSC衍生心肌细胞的功能性，适用于后续的应用与分析。该试剂盒兼容通过STEMdiff™ 心室肌细胞分化试剂盒（目录号 #05010）与STEMdiff™ 心房肌细胞分化试剂盒（目录号 #100-0215）生成的心肌细胞。
分类
专用培养基
细胞类型
心肌细胞，PSC衍生
种属
人
应用
细胞培养，培养
品牌
STEMdiff
研究领域
干细胞生物学
制剂类别
无血清
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
应用领域
本产品专为以下研究领域设计，适用于工作流程中的高亮阶段。探索这些工作流程，了解更多我们为各研究领域提供的其他配套产品。
相关材料与文献
技术资料 (7)
文献 (1)
Propionic Acidemia?Induced Proarrhythmic Electrophysiological Alterations in Human iPSC?Derived Cardiomyocytes
Journal of Inherited Metabolic Disease 2025 Apr
Abstract
ABSTRACTPropionic acidemia (PA) is a metabolic disorder caused by a deficiency of the mitochondrial enzyme propionyl?CoA carboxylase (PCC) due to mutations in the PCCA or PCCB genes, which encode the two PCC subunits. PA may lead to several types of cardiomyopathy and has been linked to cardiac electrical abnormalities such as QT interval prolongation, life?threatening arrhythmias, and sudden cardiac death. To gain insights into the mechanisms underlying PA?induced proarrhythmia, we recorded action potentials (APs) and ion currents using whole?cell patch?clamp in ventricular?like induced pluripotent stem cells?derived cardiomyocytes (hiPSC?CMs) from a PA patient carrying two pathogenic mutations in the PCCA gene (p.Cys616_Val633del and p.Gly477Glufs*9) (PCCA cells) and from a healthy subject (healthy cells). In cells driven at 1?Hz, PCC deficiency increased the latency and prolonged the AP duration (APD) measured at 20% of repolarization, without modifying resting membrane potential or AP amplitude. Moreover, delayed afterdepolarizations appeared at the end of the repolarization phase in unstimulated and paced PCCA cells. PCC deficiency significantly reduced peak sodium current (I
Na) but increased the late I
Na (I
NaL) component. In addition, L?type Ca2+ current (I
CaL) density was reduced, while the inward and outward density of the Na+/Ca2+ exchanger current (I
NCX) was increased in PCCA cells compared to healthy ones. In conclusion, our results demonstrate that at the cellular level, PCC deficiency can modify the ion currents controlling cardiac excitability, APD, and intracellular Ca2+ handling, increasing the risk of arrhythmias independently of the progressive late?onset cardiomyopathy induced by PA disease.
更多信息
| 物种 | 人类 |
|---|---|
| 配方 | 无血清 |
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