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骨骼肌中钙离子瞬变的衰减阶段:调节与生理学

The decay phase of Ca2+ transients in skeletal muscle: regulation and physiology.

作者信息

Tupling A Russell

机构信息

Department of Kinesiology, University of Waterloo, Waterloo, ON N2L 3G1, Canada.

出版信息

Appl Physiol Nutr Metab. 2009 Jun;34(3):373-6. doi: 10.1139/H09-033.

DOI:10.1139/H09-033
PMID:19448701
Abstract

Cytosolic Ca2+ transients associated with contraction and relaxation cycles in skeletal muscle are primarily dependent on the kinetics of Ca2+ release and Ca2+ uptake by the sarcoplasmic reticulum (SR). In humans, sarco(endo)plasmic reticulum Ca2+-ATPases (SERCAs) are solely responsible for the removal of Ca2+ from the cytosol following muscle contraction. There are several signalling systems involved in the acute regulation of SERCAs required to achieve a given Ca2+ transient during muscle contraction-relaxation cycles. Cyclic-AMP-dependent protein kinase and Ca2+/calmodulin-dependent protein kinase signalling activate SERCAs through the regulation of the endogenous SERCA-regulatory proteins, phospholamban and sarcolipin, both of which are highly expressed in human skeletal muscle. Recent studies on the regulation of SERCA2b in arterial smooth muscle and work from my laboratory on the interaction between SERCAs and the inducible 70-kDa heat shock protein suggests a novel role for redox signalling in regulating SERCA activity. In the absence of fatigue, activation of these signalling systems in response to repeated muscle activity serves to increase the rate of cytosolic free Ca2+ ([Ca2+]f) decay (i.e., SR Ca2+ uptake) and the speed of muscle relaxation.

摘要

与骨骼肌收缩和舒张周期相关的胞质Ca2+瞬变主要取决于肌浆网(SR)对Ca2+的释放和摄取动力学。在人类中,肌浆(内质)网Ca2+-ATP酶(SERCAs)是肌肉收缩后从胞质溶胶中清除Ca2+的唯一负责者。在肌肉收缩-舒张周期中,有几种信号系统参与了实现给定Ca2+瞬变所需的SERCAs急性调节。环磷酸腺苷依赖性蛋白激酶和Ca2+/钙调蛋白依赖性蛋白激酶信号通过调节内源性SERCA调节蛋白受磷蛋白和肌浆脂蛋白来激活SERCAs,这两种蛋白在人类骨骼肌中均高表达。最近关于动脉平滑肌中SERCA2b调节的研究以及我实验室关于SERCAs与诱导型70 kDa热休克蛋白之间相互作用的研究表明,氧化还原信号在调节SERCA活性方面具有新作用。在无疲劳的情况下,这些信号系统响应重复的肌肉活动而激活,有助于提高胞质游离Ca2+([Ca2+]f)的衰减速率(即SR对Ca2+的摄取)和肌肉舒张速度。

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