Store-operated calcium entry in differentiated C2C12 skeletal muscle cells
Store-operated calcium entry in differentiated C2C12 skeletal muscle cells
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DOI：
10.1016/j.bbamem.2005.02.017
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发表时间：
2005-06-01
影响因子：
3.4
通讯作者：
Henao, F
中科院分区：
文献类型：
--
作者：
Gutierrez-Martin, Y;Martin-Romero, FJ;Henao, F
在本文中，我们进一步证明了在肌浆网Ca2+-ATP酶抑制剂thapsigargin、ryanodine受体激活剂咖啡因和激活嘌呤能受体的ATP，在肌浆网Ca2+耗尽后，分化的骨骼肌C2C12肌管中存在储存操作的钙进入。Mn2+对fura 2荧光发射的猝灭也为储存操作钙进入提供了证据，因为当肌浆网Ca2+耗尽时，这种猝灭会加速。Ca2+进入对Ni2+、La3+、Gd3+和2-氨基乙基二苯硼酸盐敏感，但对硝苯地平耐药，因此排除了l型Ca2+通道。我们使用ATP进行存储损耗获得的数据表明，内部存储中的Ca2+水平可能在这种细胞类型的存储操作钙通道活性调节中发挥作用。(c) 2005 Elsevier B.V.版权所有
In this paper, we show further evidences for the existence of store-operated calcium entry in differentiated skeletal muscle C2C12 myotubes after Ca2+ depletion in sarcoplasmic reticulum, using thapsigargin, a potent sarcoplasmic reticulum Ca2+-ATPase inhibitor, caffeine as ryanodine receptor activator, and ATP which activates purinergic receptors. The quenching of fura 2 fluorescence emission by Mn2+ also provided evidences for store-operated calcium entry because this quenching was accelerated when sarcoplasmic reticulum was depleted of Ca2+. Ca2+ entry was sensitive to Ni2+, La3+, Gd3+ and 2-aminoethyl diphenyl borate but resistant to nifedipine, thus excluding L-type Ca2+ channels in this type of calcium entry. Our data obtained using ATP for store depletion suggest that the level of Ca2+ in internal stores could play a role in the regulation of store-operated calcium channel activity in this cell type. (c) 2005 Elsevier B.V. All rights reserved.