Homocysteine inhibits store-mediated calcium entry in human endothelial cells: Evidence for involvement of membrane potential and actin cytoskeleton

被引:1
作者
Hong-Sheng Zhang
Jun-Hua Xiao
En-Hua Cao
Jin-Fen Qin
机构
[1] Institute of Biophysics,Center for System Biology
[2] Huazhong University of Science & Technology,Department of Pharmacology, Tongji Medical College
[3] Institute of Biophysics,Center for System Biology
来源
Molecular and Cellular Biochemistry | 2005年 / 269卷
关键词
actin cytoskeleton; BK; channels; capacitative Ca; entry; homocysteine; membrane potential;
D O I
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中图分类号
学科分类号
摘要
The role of homocysteine for store-operated calcium influx was investigated in human umbilical cord endothelial cell line. Homocysteine significantly decreased thapsigargin-evoked Ca2+ entry, membrane hyperpolarization and actin polymerization. GSH and DTT prevented homocysteine-induced inhibition of thapsigargin-evoked Ca2+ entry, membrane hyperpolarization and actin polymerization; while GSSG had the opposite effect. Homocysteine blocked large conductance Ca2+-activated K+ (BKCa) channels in a concentration-dependent manner and related to the redox status of the endothelial cells. BKCa channels opener NS1619 reversed thapsigargin-evoked Ca2+ entry, membrane hyperpolarization and actin polymerization; BKCa channels inhibitor iberiotoxin had the opposite effect. The findings suggest that homocysteine is involved in store-regulated Ca2+ entry through membrane potential-dependent and actin cytoskeleton-dependent mechanisms, redox status of homocysteine and BKCa channels may play a regulatory role in it. (Mol Cell Biochem 269: 37–47, 2005)
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页码:37 / 47
页数:10
相关论文
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