Conformational activation of Ca2+ entry by depolarization of skeletal myotubes
Conformational activation of Ca2+ entry by depolarization of skeletal myotubes
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DOI：
10.1073/pnas.0403485101
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发表时间：
2004-11-02
影响因子：
11.1
通讯作者：
Pessah, IN
中科院分区：
文献类型：
--
作者：
Cherednichenko, G;Hurne, AM;Pessah, IN
钙库操纵的钙内流（SOCE）发生在不同类型的细胞中，以响应内质网/肌浆网内钙的耗竭，并起到重新填充这些钙库和塑造细胞质钙瞬变的作用。在这里，我们报告说，除了传统的SOCE，骨骼肌肌管显示的生理机制，我们术语兴奋耦合钙离子内流（ECCE）。ECCE通过膜去极化迅速启动。像兴奋-收缩偶联一样，ECCE在缺乏骨骼肌型兰尼碱受体1的发育不良肌管和缺乏二氢吡啶受体（DHPR）的发育不良肌管中均不存在，并且独立于DHPR L型Ca 2+电流。与经典的SOCE不同，ECCE不依赖于肌浆网Ca 2+释放。事实上，ECCE产生一个大的Ca 2+进入响应于生理刺激，不产生实质性的存储耗尽，并依赖于三个不同的Ca 2+通道之间的相互作用：DHPR，ryanodine受体1，和Ca 2+进入通道与存储操作的Ca 2+通道的属性相对应。ECCE可以提供一种基本的手段，以快速维持Ca 2+商店和控制的重要方面的Ca 2+信号在肌肉和非肌肉细胞。
Store-operated Ca2+ entry (SOCE) occurs in diverse cell types in response to depletion of Ca2+ within the endoplasmic/sarcoplasmic reticulum and functions both to refill these stores and to shape cytoplasmic Ca2+ transients. Here we report that in addition to conventional SOCE, skeletal myotubes display a physiological mechanism that We term excitation-coupled Ca2+ entry (ECCE). ECCE is rapidly initiated by membrane depolarization. Like excitation-contraction coupling, ECCE is absent in both dyspedic myotubes that lack the skeletal muscle-type ryanodine receptor 1 and dysgenic myotubes that lack the dihydropyridine receptor (DHPR), and is independent of the DHPR L-type Ca2+ current. Unlike classic SOCE, ECCE does, not depend on sarcoplasmic reticulum Ca2+ release. Indeed, ECCE produces a large Ca2+ entry in response to physiological stimuli that do not produce substantial store depletion and depends on interactions among three different Ca2+ channels: the DHPR, ryanodine receptor 1, and a Ca2+ entry channel with properties corresponding to those of store-operated Ca2+ channels. ECCE may provide a fundamental means to rapidly maintain Ca2+ stores and control important aspects of Ca2+ Signaling in both muscle and nonmuscle cells.