| Literature DB >> 15786715 |
Hong-Sheng Zhang1, Jun-Hua Xiao, En-Hua Cao, Jin-Fen Qin.
Abstract
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+ (BK(Ca)) channels in a concentration-dependent manner and related to the redox status of the endothelial cells. BK(Ca) channels opener NS1619 reversed thapsigargin-evoked Ca2+ entry, membrane hyperpolarization and actin polymerization; BK(Ca) 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 BK(Ca) channels may play a regulatory role in it.Entities:
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Year: 2005 PMID: 15786715 DOI: 10.1007/s11010-005-3168-z
Source DB: PubMed Journal: Mol Cell Biochem ISSN: 0300-8177 Impact factor: 3.396