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In vitro cell stretching technology (IsoStretcher) as an approach to unravel Piezo1-mediated cardiac mechanotransduction.
Progress in Biophysics and Molecular Biology ( IF 3.8 ) Pub Date : 2020-08-05 , DOI: 10.1016/j.pbiomolbio.2020.07.003
Yang Guo 1 , Anna-Lena Merten 2 , Ulrike Schöler 2 , Ze-Yan Yu 1 , Jasmina Cvetkovska 3 , Diane Fatkin 4 , Michael P Feneley 5 , Boris Martinac 6 , Oliver Friedrich 7
Affiliation  

The transformation of electrical signals into mechanical action of the heart underlying blood circulation results in mechanical stimuli during active contraction or passive filling distention, which conversely modulate electrical signals. This feedback mechanism is known as cardiac mechano-electric coupling (MEC). The cardiac MEC involves complex activation of mechanical biosensors initiating short-term and long-term effects through Ca2+ signals in cardiomyocytes in acute and chronic pressure overload scenarios (e.g. cardiac hypertrophy). Although it is largely still unknown how mechanical forces alter cardiac function at the molecular level, mechanosensitive channels, including the recently discovered family of Piezo channels, have been thought to play a major role in the cardiac MEC and are also suspected to contribute to development of cardiac hypertrophy and heart failure. The earliest reports of mechanosensitive channel activity recognized that their gating could be controlled by membrane stretch. In this article, we provide an overview of the stretch devices, which have been employed for studies of the effects of mechanical stimuli on muscle and heart cells. We also describe novel experiments examining the activity of Piezo1 channels under multiaxial stretch applied using polydimethylsiloxane (PDMS) stretch chambers and IsoStretcher technology to achieve isotropic stretching stimulation to cultured HL-1 cardiac muscle cells which express an appreciable amount of Piezo1.



中文翻译:

体外细胞拉伸技术 (IsoStretcher) 作为解开 Piezo1 介导的心脏机械转导的一种方法。

电信号转化为心脏基础血液循环的机械作用导致主动收缩或被动充盈膨胀期间的机械刺激,其反过来调节电信号。这种反馈机制被称为心脏机电耦合 (MEC)。心脏 MEC 涉及机械生物传感器的复杂激活,通过 Ca 2+启动短期和长期影响急性和慢性压力超负荷情况下的心肌细胞信号(例如心脏肥大)。尽管在分子水平上机械力如何改变心脏功能在很大程度上仍然未知,但机械敏感通道,包括最近发现的压电通道家族,已被认为在心脏 MEC 中起主要作用,并且也被怀疑有助于发展心脏肥大和心力衰竭。机械敏感通道活动的最早报告认识到它们的门控可以通过膜拉伸来控制。在本文中,我们概述了拉伸装置,这些装置已被用于研究机械刺激对肌肉和心脏细胞的影响。IsoStretcher技术实现对培养的 HL-1 心肌细胞的各向同性拉伸刺激,这些细胞表达可观的 Piezo1。

更新日期:2020-08-05
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