Inhibition of osteoblast differentiation by aluminum trichloride exposure is associated with inhibition of BMP-2/Smad pathway component expression
Inhibition of osteoblast differentiation by aluminum trichloride exposure is associated with inhibition of BMP-2/Smad pathway component expression
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三氯化铝暴露对成骨细胞分化的抑制与 BMP-2/Smad 通路成分表达的抑制有关
DOI：
10.1016/j.fct.2016.09.004
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发表时间：
2016
影响因子：
4.3
通讯作者：
Zhu Yanzhu
中科院分区：
文献类型：
--
作者：
Yang Xu;Huo Hui;Xiu Chunyu;Song Miao;Han Yanfei;Li Yanfei;Zhu Yanzhu
骨形态发生蛋白-2（BMP-2）/Smad信号通路在成骨细胞（OB）分化的调控中起重要作用。成骨细胞分化是骨形成的关键过程。铝（Al）暴露抑制骨形成并导致Al诱导的骨疾病。然而，该机制尚未完全理解。为探讨BMP-2/Smad信号通路是否与AlCl 3处理的成骨细胞分化有关，将原代培养的大鼠成骨细胞分别暴露于0（对照组，CG）、1/40 IC 50（低剂量组，LG）、1/20 IC 50（中剂量组，MG）和1/10 IC 50（高剂量组，HG）24 h。结果发现，与对照组相比，AlCl 3处理组OB分化标志物（Runx-2、Osterix和ALP）和BMP-2/Smad信号通路组分（BMP-2、BMPR-IA、p-BMPR-IA、BMPR-II、p-Smad 1/5/8和p-Smad 1/5/8/4）的表达均降低。这些结果表明AlCl 3抑制成骨细胞分化与抑制BMP-2/Smad通路组分的表达有关。我们的研究结果提供了一个新的见解AlCl 3诱导的骨疾病的机制。
Bone morphogenetic protein-2 (BMP-2)/Smad signaling pathway plays an important role in regulating osteoblast (OB) differentiation. OB differentiation is a key process of bone formation. Aluminum (Al) exposure inhibits bone formation and causes Al-induced bone disease. However, the mechanism is not fully understood. To investigate whether BMP-2/Smad signaling pathway is associated with OB differentiation in aluminum trichloride (AlCl3)-treated OBs, the primary rat OBs were cultured and exposed to 0 (control group, CG), 1/40 IC50(low-dose group, LG), 1/20 IC50(mid-dose group, MG), and 1/10 IC50(high-dose group, HG) of AlCl3for 24 h, respectively. We found that the expressions of OB differentiation markers (Runx-2, Osterix and ALP) and BMP-2/Smad signaling pathway components (BMP-2, BMPR-IA, p-BMPR-IA, BMPR-II, p-Smad1/5/8 and p-Smad1/5/8/4) were all decreased in AlCl3-treated OBs compared with the CG. These results indicated that inhibition of OB differentiation by AlCl3was associated with inhibition of BMP-2/Smad pathway component expression. Our findings provide a novel insight into the mechanism of AlCl3-induced bone disease.