Bone morphogenetic protein 7 attenuates epithelial-mesenchymal transition induced by silica

作者：Yang, G.; Zhu, Z.; Wang, Y.; Gao, A.; Niu, P.; Chen, L.; Tian, L.^*

来源：Human & Experimental Toxicology, 2016, 35(1): 69-77.

DOI：10.1177/0960327115577550

• Bone morphogenetic protein-7
• epithelial-mesenchymal transition
• pulmonary fibrosis
• silica

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.

• 出版日期2016-1
• 单位首都医科大学