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首页> 外文期刊>Cellular Physiology and Biochemistry >Functional Characterization of Inward Rectifier Potassium Ion Channel in Murine Fetal Ventricular Cardiomyocytes
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Functional Characterization of Inward Rectifier Potassium Ion Channel in Murine Fetal Ventricular Cardiomyocytes

机译:小鼠胎儿心室心肌细胞内向整流钾离子通道的功能表征

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摘要

Aims: Previous studies have shown the dramatic changes in electrical properties of murine fetal cardiomyocytes, while details on inward rectifier potassium current (IK1) are still seldom discussed. Thus we aimed to characterize the functional expression and functional role of IK1 in murine fetal ventricular cardiomyocytes. Methods: Whole cell patch clamp was applied to investigate the electrophysiological properties of IK1. Quantitative real-time PCR, western blotting and double-label immunofluorescence were further utilized to find out the molecular basis of IK1. Results: Compared to early developmental stage (EDS), IK1 at late developmental stage (LDS) displayed higher current density, stronger rectifier property and faster activation kinetics. It was paralleled with the downregulation of Kir2.3 and the upregulation of Kir2.1/Kir2.2. IK1 contributed to maintain the maximum diastolic potential (MDP), late repolarization phase (LRP) as well as the action potential duration (APD). However, the contribution to MDP and velocity of LRP did not change significantly with maturation. Conclusions: During fetal development, the switch of IK1 subtypes from Kir2.1/Kir2.3 to Kir2.1 resulted in the dramatic changes in IK1 electrophysiological properties.
机译:目的:先前的研究表明,鼠胎儿心肌细胞的电特性发生了巨大变化,而关于内向整流钾电流(IK1)的细节仍然很少讨论。因此,我们旨在表征IK1在鼠胎儿心室心肌细胞中的功能表达和功能作用。方法:应用全细胞膜片钳研究IK1的电生理特性。进一步利用实时荧光定量PCR,蛋白质印迹和双标记免疫荧光来发现IK1的分子基础。结果:与早期发育阶段(EDS)相比,晚期发育阶段(LDS)的IK1显示出更高的电流密度,更强的整流特性和更快的活化动力学。它与Kir2.3的下调和Kir2.1 / Kir2.2的上调同时进行。 IK1有助于维持最大舒张电位(MDP),晚期复极化阶段(LRP)以及动作电位持续时间(APD)。但是,对MDP的贡献和LRP的速度不会随着成熟而显着变化。结论:在胎儿发育过程中,IK1亚型从Kir2.1 / Kir2.3转变为Kir2.1导致IK1电生理特性发生了巨大变化。

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