Calcium-dependent facilitation and graded deactivation of store-operated calcium entry in fetal skeletal muscle

被引:18
作者
Collet, C [1 ]
Ma, JJ [1 ]
机构
[1] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Physiol & Biophys, Piscataway, NJ 08854 USA
关键词
D O I
10.1529/biophysj.103.039305
中图分类号
Q6 [生物物理学];
学科分类号
071011 ;
摘要
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.
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页码:268 / 275
页数:8
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