Calcium-dependent facilitation and graded deactivation of store-operated calcium entry in fetal skeletal muscle
Calcium-dependent facilitation and graded deactivation of store-operated calcium entry in fetal skeletal muscle
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DOI：
10.1529/biophysj.103.039305
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发表时间：
2004-07-01
影响因子：
3.4
通讯作者：
Ma, JJ
中科院分区：
文献类型：
--
作者：
Collet, C;Ma, JJ
激活钙库操纵的 Ca2+ 进入细胞质 (SOCE) 需要来自细胞内 Ca2+ 释放机制的逆行信号传导，该过程涉及细胞内膜和细胞表面膜上的蛋白质成分之间的密切相互作用。肌肉细胞中控制 Ca2+ 运动的细胞机制受到发育调节，反映了连接膜结构的成熟以及相关 Ca2+ 信号分子的协调表达。在这里，我们证明了从小鼠胚胎第 15 天和第 16 天（肌肉发育的关键阶段）获得的新鲜分离的骨骼肌细胞中存在 SOCE。随着 Ca2+ 被肌浆网 (SR) 吸收，胎儿肌肉中的 SOCE 逐渐失活。在短暂暴露于高胞质 Ca2+ 的细胞中观察到一种新的 Ca2+ 依赖性 SOCE 促进作用。我们的数据表明，胞质 Ca2+ 可以促进 SOCE，而 SR 管腔 Ca2+ 可以使胎儿骨骼肌中的 SOCE 失活。这种 Ca2+ 离子调节 SOCE 的协同机制不仅能够通过 SR 膜严格控制 SOCE，而且还提供了一种响应生理需求的细胞外 Ca2+ 进入的有效机制。这种 Ca2+ 信号传导机制可能有助于胎儿骨骼肌的收缩和发育。
Activation of store-operated Ca2+ entry ( SOCE) into the cytoplasm requires retrograde signaling from the intracellular Ca2+ release machinery, a process that involves an intimate interaction between protein components on the intracellular and cell surface membranes. The cellular machinery that governs the Ca2+ movement in muscle cells is developmentally regulated, reflecting maturation of the junctional membrane structure as well as coordinated expression of related Ca2+ signaling molecules. Here we demonstrate the existence of SOCE in freshly isolated skeletal muscle cells obtained from embryonic days 15 and 16 of the mouse embryo, a critical stage of muscle development. SOCE in the fetal muscle deactivates incrementally with the uptake of Ca2+ into the sarcoplasmic reticulum (SR). A novel Ca2+-dependent facilitation of SOCE is observed in cells transiently exposed to high cytosolic Ca2+. Our data suggest that cytosolic Ca2+ can facilitate SOCE whereas SR luminal Ca2+ can deactivate SOCE in the fetal skeletal muscle. This cooperative mechanism of SOCE regulation by Ca2+ ions not only enables tight control of SOCE by the SR membrane, but also provides an efficient mechanism of extracellular Ca2+ entry in response to physiological demand. Such Ca2+ signaling mechanism would likely contribute to contraction and development of the fetal skeletal muscle.