Bone morphogenetic protein 7 attenuates epithelial–mesenchymal transition induced by silica
Bone morphogenetic protein 7 attenuates epithelial–mesenchymal transition induced by silica
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DOI：
10.1177/0960327115577550
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发表时间：
2016-01
影响因子：
2.8
通讯作者：
G. Yang;Z. Zhu;Y. Wang;A. Gao;P. Niu;L. Chen;L. Tian
中科院分区：
文献类型：
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作者：
G. Yang;Z. Zhu;Y. Wang;A. Gao;P. Niu;L. Chen;L. Tian
上皮-间质转化（EMT）是肺纤维化的关键过程。骨形态发生蛋白7（BMP-7）能够逆转近端肾小管上皮细胞的EMT。因此，我们测试的假设，EMT有助于二氧化硅诱导的肺纤维化和BMP-7抑制EMT二氧化硅诱导的肺纤维化。采用大鼠进行性矽肺纤维化模型。从大鼠纤维化肺测量上皮和间质标志物。然后在A549细胞中进一步证实BMP-7对EMT的影响。在暴露于二氧化硅的大鼠肺中，作为间充质标志物的波形蛋白增加，作为上皮标志物的E-钙粘蛋白减少，这与A549细胞数据一致。然而，BMP-7治疗显著降低大鼠肺纤维化模型和A549细胞中波形蛋白的表达。总之，EMT有助于二氧化硅诱导的肺纤维化。同时，BMP-7在体内外均能抑制二氧化硅诱导的EMT。
The epithelial–mesenchymal transition (EMT) is a critical process in the pulmonary fibrosis. It has been reported that bone morphogenetic protein 7 (BMP-7) was able to reverse EMT in proximal tubular cells. Therefore, we test the hypothesis that EMT contributes to silica-induced pulmonary fibrosis and BMP-7 inhibits EMT in silica-induced pulmonary fibrosis. Progressive silica-induced pulmonary fibrosis in the rat was used as a model of silicosis. Epithelial and mesenchymal markers were measured from rat fibrotic lungs. Then the effects of BMP-7 on the EMT were further confirmed in A549 cells. There are increases of vimentin as a mesenchymal marker and decreases of E-cadherin as an epithelial marker in the silica-exposed rat lungs, which is in agreement with the A549 cells data. However, BMP-7 treatment significantly reduced expression of vimentin in the rat pulmonary fibrosis model and in A549 cells. In conclusion, EMT contributes to silica-induced pulmonary fibrosis. Meanwhile, the treatment of BMP-7 can inhibit silica-induced EMT in vitro and in vivo.