Aluminum Trichloride Inhibited Osteoblastic Proliferation and Downregulated the Wnt/beta-Catenin Pathway

文献类型： 外文期刊

第一作者： Huang, Wanyue

作者： Huang, Wanyue;Wang, Peiyan;Shen, Tongtong;Han, Yanfei;Song, Miao;Bian, Yu;Li, Yanfei;Hu, Chongwei;Zhu, Yanzhu

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关键词： Aluminum trichloride;Osteoblastic proliferation;Wnt/beta-catenin signaling pathway;Rat osteoblasts

期刊名称：BIOLOGICAL TRACE ELEMENT RESEARCH （ 影响因子：3.738； 五年影响因子：3.44 ）

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收录情况： SCI

摘要： Aluminum (Al) exposure inhibits bone formation. Osteoblastic proliferation promotes bone formation. Therefore, we inferred that Al may inhibit bone formation by the inhibition of osteoblastic proliferation. However, the effects and molecular mechanisms of Al on osteoblastic proliferation are still under investigation. Osteoblastic proliferation can be regulated by Wnt/beta-catenin signaling pathway. To investigate the effects of Al on osteoblastic proliferation and whether Wnt/beta-catenin signaling pathway is involved in it, osteoblasts from neonatal rats were cultured and exposed to 0, 0.4 mM (1/20 IC50), 0.8 mM (1/10 IC50), and 1.6 mM (1/5 IC50) of aluminum trichloride (AlCl3) for 24 h, respectively. The osteoblastic proliferation rates; Wnt3a, lipoprotein receptor-related protein 5 (LRP-5), T cell factor 1 (TCF-1), cyclin D1, and c-Myc messenger RNA (mRNA) expressions; and p-glycogen synthase kinase 3 beta (GSK3 beta), GSK3 beta, and beta-catenin protein expressions indicated that AlCl3 inhibited osteoblastic proliferation and downregulated Wnt/beta-catenin signaling pathway. In addition, the AlCl3 concentration was negatively correlated with osteoblastic proliferation rates and the mRNA expressions of Wnt3a, c-Myc, and cyclin D1, while the osteoblastic proliferation rates were positively correlated with mRNA expressions of Wnt3a, c-Myc, and cyclin D1. Taken together, these findings indicated that AlCl3 inhibits osteoblastic proliferation may be associated with the inactivation of Wnt/beta-catenin signaling pathway.

分类号： Q5

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