ZIP1 and Zinc Inhibits Fluoride-Induced Apoptosis in MC3T3-E1 Cells

被引:23
作者
Xu, Shihong [1 ]
Yang, Yongliang [1 ]
Han, Shumei [2 ]
Wu, Zonghui [3 ]
机构
[1] Shandong Univ, Shandong Prov Hosp, Dept Orthopaed, Jinan 250021, Shandong, Peoples R China
[2] Shandong Canc Hosp & Inst, Dept Med, Jinan 250117, Shandong, Peoples R China
[3] Shandong Univ, Shandong Med Imaging Res Inst, Dept Ultrasound Diag, Jinan 250021, Shandong, Peoples R China
关键词
Zinc; Fluoride; Apoptosis; ROS; ZIP1; OXIDATIVE STRESS; BONE-FORMATION; SUPPLEMENTATION; DIFFERENTIATION; PROLIFERATION; ACTIVATION; EXPRESSION; OSTEOBLAST; AUTOPHAGY; TOXICITY;
D O I
10.1007/s12011-014-9935-5
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Excess fluoride intake could induce apoptosis in the cells. As an essential micronutrient and cytoprotectant, zinc is involved in many types of apoptosis. Here, we studied the effects of zinc and ZIP1 on fluoride-induced apoptosis in mouse MC3T3-E1 cells and examined the underlying molecular mechanisms. Our study found that fluoride not only inhibited cell proliferation and increased the intracellular reactive oxygen species (ROS) but also induced cell apoptosis. Whereas pretreatment with zinc significantly attenuated fluoride-induced ROS production and partly protected cells against fluoride-induced apoptosis through MAPK/ERK signaling pathway. Our study also found that fluoride upregulated the expression of ZIP1 in a time-dependent manner. Moreover, overexpression of ZIP1 also inhibited fluoride-induced apoptosis by activation of PI3K/Akt pathway. This cytoprotective effect of zinc and ZIP1 may be new factors that affect the physiological activity of fluoride and need study further.
引用
收藏
页码:399 / 409
页数:11
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