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

被引：13

作者：

Zhang, HS

Xiao, JH

Cao, EH

Qin, JF

机构：

[1] Acad Sinica, Inst Biophys, Ctr Syst Biol, Beijing 100101, Peoples R China

[2] Huazhong Univ Sci & Technol, Tongji Med Coll, Dept Pharmacol, Wuhan 430074, Peoples R China

来源：

MOLECULAR AND CELLULAR BIOCHEMISTRY | 2005年 / 269卷 / 1-2期

基金：

中国国家自然科学基金;

关键词：

actin cytoskeleton; BKCa channels; capacitative Ca2+ entry; homocysteine; membrane potential;

D O I：

10.1007/s11010-005-3168-z

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

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.

引用

页码：37 / 47

页数：11

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