机构：[a]Molecular Medicine Center, the Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, China[b]Department of Molecular Diagnostics and Biopharmaceutics, College of Pharmacy, Soochow University, Suzhou, Jiangsu 215004, China[c]CHUL Research Center, Laval University, Quebec, Canada G1V 4G2
Hepcidin is a key player in the regulation of iron homeostasis. Several pathological conditions associated with iron overload are attributed to the depressed expression of hepcidin and are often associated with bone diseases including osteoporosis. Hepcidin was suggested to have anti-osteoporosis effects by preventing iron overload. We recently observed that hepcidin could increase intracellular calcium concentration in cultured osteoblast cells. The present study was designed to elucidate the source of the increased intracellular calcium following hepcidin activation. Cultured hFOB1.19 cells were used to test whether there was a dose dependent effect of hepcidin on increasing intracellular calcium. After finding the optimal concentration in increasing intracellular calcium, Cultured hFOB1.19 cells were then divided into three groups: (1) control group, (2) and (3) groups pretreated with either nimodipine (2 x 10(-5) mol/L) or EDTA (2 x 10(-3) mol/L) for 10 min before incubation with hepcidin (100 nmol/L). All cells were stimulated with hepcidin for 60 min and then stained with fluo-3/AM for 40 min before the intracellular calcium was observed using flow cytometry (FCM). As compared with controls, hepcidin treatment significantly increased intracellular calcium concentration. This effect was blocked by nimodipine and EDTA pretreatments which suggested that hepcidin-mediated calcium inflow was mainly through L-type Ca2+ channels and that the release of intracellular calcium store was not significant. Hepcidin increases of intracellular calcium may be related to its anti-osteoporosis effect but this hypothesis needs further investigation. (C) 2011 Elsevier B.V. All rights reserved.
基金：
This study was partially supported by the Jiangsu provincial grants
BK2008165 and RC2007100.
第一作者机构：[a]Molecular Medicine Center, the Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, China[b]Department of Molecular Diagnostics and Biopharmaceutics, College of Pharmacy, Soochow University, Suzhou, Jiangsu 215004, China
通讯作者：
通讯机构：[a]Molecular Medicine Center, the Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, China[b]Department of Molecular Diagnostics and Biopharmaceutics, College of Pharmacy, Soochow University, Suzhou, Jiangsu 215004, China
推荐引用方式(GB/T 7714)：
Youjia Xu,Guangfei Li,Bencai Du,et al.Hepcidin increases intracellular Ca2+ of osteoblast hFOB1.19 through L-type Ca2+ channels[J].REGULATORY PEPTIDES.2011,172(1-3):58-61.doi:10.1016/j.regpep.2011.08.009.
APA：
Youjia Xu,Guangfei Li,Bencai Du,Peng Zhang,Li Xiao...&Kai Li.(2011).Hepcidin increases intracellular Ca2+ of osteoblast hFOB1.19 through L-type Ca2+ channels.REGULATORY PEPTIDES,172,(1-3)
MLA：
Youjia Xu,et al."Hepcidin increases intracellular Ca2+ of osteoblast hFOB1.19 through L-type Ca2+ channels".REGULATORY PEPTIDES 172..1-3(2011):58-61
