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

Human & Experimental Toxicology
Gengxia YangLin Tian

Abstract

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.

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Citations

May 10, 2017·Developmental Dynamics : an Official Publication of the American Association of Anatomists·Kumi ShiraiShizuya Saika
Sep 30, 2016·Medical Science Monitor : International Medical Journal of Experimental and Clinical Research·Xinjun ChenDanping Liu
Nov 24, 2019·Seminars in Cell & Developmental Biology·Jason S RockelSowmya Viswanathan
Mar 27, 2021·Frontiers in Cell and Developmental Biology·Shengnan YangChen Wang

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Methods Mentioned

BETA
electrophoresis

Software Mentioned

SPSS
Pro Plus
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