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Ca2+ spark dynamics in cardiac myocyte

机译:CA2 +心肌细胞中的火花动态

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Ca2+, one of the most classical messengers in living cells, regulates many important life processes, from hormone secretion to muscle contraction, nerve signal transduction to learning and memory, gene expression to protein phosphorylation. But how can Ca2+ take on such a wide range of physiological functions? The relations among these functions, sorts of Ca2+ channels, space distribution, kinetic control, and Ca2+ buffering and diffusion in cell microenvironment, are essential problems for research on Ca2+ signal transduction and important foundation for elucidating cell function, growth, signal process and pathology. Cheng et al. first demonstrated that Ca2+ release from the sarcoplasmic reticulum (SR) occurs as discrete quanta[1]. They named these quanta Ca2+ sparks because of the brief localized light emission they induced in Ca2+sensitive fluorescent dyes. Since their discovery, Ca2+ sparks have been found in cardiac, skeletal, and smooth muscle cells and provide molecular interpretations for intercellular Ca2+ signal transduction[2-4]. However, in the opinion of biomechanics, Ca2+ spark is a dynamic process of random point source diffusion and chemical reactions of substances in the cell. The classical Fickian diffusion e-quation and reaction-kinetic model have been widely used to describe the process. However, recent work suggests that even the minimum spatial scale of Ca2+ spark is still much larger than that simulated by the Fickian diffusion model [5]. Based on the diffusion phenomenon of Ca2+ spark in cardiac myocytes, an essential question on unit calcium signal has been put forward: whether the diffusion of calcium spark obeys Fickian diffusion, if not, why? Furthermore, which rule and theory can best describe kinetics of this anomalous diffusion. These are very important to elucidate how Ca2+ molecular channel produces gradient of calcium signal, how different gradients activate different target sites and downstream signal pathway, and consequently control different life process in the cell.
机译:CA2 +,活细胞中最古典信使之一,调节许多重要的生命过程,从激素分泌到肌肉收缩,神经信号转导对学习和记忆,基因表达到蛋白质磷酸化。但CA2 +如何承担如此广泛的生理功能?这些功能的关系,分类的CA2 +通道,空间分布,动力控制和CA2 +缓冲以及细胞微环境中的扩散,对CA2 +信号转导和阐明细胞功能,生长,信号过程和病理学的重要基础进行了重要问题。程等人。首先证明了来自肌肉网(SR)的Ca2 +释放作为离散量子[1]发生。它们由于在Ca2 +敏感荧光染料中诱导的简要局部光发射而命名为这些量子CA2 +火花。自发现以来,已在心脏,骨骼和平滑肌细胞中发现CA2 +火花,并为细胞间CA2 +信号转导提供分子解释[2-4]。然而,在生物力学的意见中,CA2 + Spark是一种动态的液体点源扩散和细胞中物质的化学反应的动态过程。经典的Fickian扩散电子官方和反应动力学模型已被广泛用于描述该过程。然而,最近的工作表明,即使是CA2 + Spark的最小空间量表仍然比Fickian扩散模型模拟的最小空间尺寸大得多[5]。基于CA2 + Spark中的扩散现象心肌细胞,提出了一项关于单位钙信号的必要问题:钙的扩散是钙Spark Obeys Fickian扩散,如果没有,为什么?此外,哪种规则和理论可以最好地描述这种异常扩散的动力学。这些非常重要的是阐明Ca2 +分子通道如何产生钙信号的梯度,不同的梯度如何激活不同的靶位点和下游信号途径,并因此控制细胞中的不同生命过程。

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