Aluminum Induces Osteoblast Apoptosis Through the Oxidative Stress-Mediated JNK Signaling Pathway
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  • 作者:Xinwei Li (1) (2)
    Yanfei Han (2)
    Yuan Guan (1)
    Liang Zhang (1)
    Chongsheng Bai (2)
    Yanfei Li (2)
  • 关键词:Aluminum ; Bone formation ; Osteoblasts ; Apoptosis ; c ; Jun N ; terminal kinase signaling pathway
  • 刊名:Biological Trace Element Research
  • 出版年:2012
  • 出版时间:December 2012
  • 年:2012
  • 卷:150
  • 期:1-3
  • 页码:502-508
  • 全文大小:292KB
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  • 作者单位:Xinwei Li (1) (2)
    Yanfei Han (2)
    Yuan Guan (1)
    Liang Zhang (1)
    Chongsheng Bai (2)
    Yanfei Li (2)

    1. College of Animal Science and Veterinary Medicine, Jilin University, 5333 Xi鈥檃n Road, Changchun, Jilin, 130062, China
    2. College of Veterinary Medicine, Northeast Agricultural University, No. 59 Mucai Street, Xiangfang District, Harbin, 150030, China
文摘
Aluminum (Al) is considered to be a potentially toxic metal. Al exposure inhibits bone formation. Few studies have investigated the mechanism of inhibitory effects of Al on bone formation. Thus, in this study, osteoblasts were cultured and exposed to different concentrations of Al to investigate the mechanism behind the inhibitory effects of Al on bone formation. Al-treated osteoblasts showed signs of oxidative stress and a high apoptosis rate. The levels of osteoblasts activity markers (bone gamma-carboxyglutamic acid protein and bone alkaline phosphatase) were significantly lower in the Al-treated groups than in the control group. The c-Jun N-terminal kinase (JNK), a major signaling pathway in regulating cell apoptosis, was activated. The phosphorylation state of JNK was significantly increased. The mRNA and protein expression of c-Jun were both significantly upregulated. The pro-apoptotic genes (caspase 3, caspase 9, bax, and factor-related apoptosis ligand) were significantly increased. However, Bcl-2, an anti-apoptotic gene, was significantly decreased. In conclusion, the results of this study indicate that Al induces osteoblast apoptosis by activating the oxidative stress-mediated JNK pathway, which causes cell injuries and reduces the number and function of osteoblasts, thereby inhibiting bone formation.

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