Capacitative calcium entry is inhibited in vascular endothelial cells by disruption of cytoskeletal microfilaments
Capacitative calcium entry is inhibited in vascular endothelial cells by disruption of cytoskeletal microfilaments
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DOI：
10.1016/s0014-5793(97)00051-3
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发表时间：
1997-02-17
期刊：
影响因子：
3.5
通讯作者：
Blatter, LA
中科院分区：
文献类型：
--
作者：
Holda, JR;Blatter, LA
完整的细胞骨架在单培养血管内皮细胞中对储存操作（“容性”）Ca2+内流的作用进行了研究。通过thapsigargin耗尽Ca2+储存诱导的细胞质Ca2+浓度（[Ca2+](i)）的变化来测量容性Ca2+进入。细胞松弛素D是一种破坏细胞骨架微丝网络的物质，经FITC-phalloidin染色证实，细胞松弛素D预处理后，Ca2+进入被抑制，细胞松弛素D不影响基础[Ca2+](i)，也不影响atp诱导的[Ca2+](i)的增加，表明Ca2+通过肌醇-磷酸盐途径从细胞内储存释放是完整的。这些结果表明微丝是容性Ca2+进入机制的一个组成部分。完整细胞骨架的必要性有利于存储操作的Ca2+内流的构象耦合模型。(C)欧洲生化学会联合会。
The role of an intact cytoskeleton for store-operated ('capacitative') Ca2+ influx was investigated in single cultured vascular endothelial cells. Capacitative Ca2+ entry was measured as changes of cytoplasmic Ca2+ concentration ([Ca2+](i)) induced by depletion of Ca2+ stores with thapsigargin. In cells pretreated with cytochalasin D, an agent that disrupts the microfilament network of the cytoskeleton, as confirmed with FITC-phalloidin staining, capacitative Ca2+ entry was inhibited, Cytochalasin D did not affect basal [Ca2+](i) nor ATP-induced increases of [Ca2+](i), indicating that release of Ca2+ from intracellular stores through the inositol-phosphate pathway was intact. These results suggest that microfilaments are an integral part of the mechanism for capacitative Ca2+ entry. The necessity for an intact cytoskeleton favors a conformational coupling model for store-operated Ca2+ influx. (C) Federation of European Biochemical Societies.