Bone morphogenetic protein 7 attenuates epithelial-mesenchymal transition induced by 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.
School of Public Health, Capital Medical University, Beijing, China Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China These authors contributed equally to this work.
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Yang
School of Public Health, Capital Medical University, Beijing, China Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China These authors contributed equally to this work.
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Zhu
School of Public Health, Capital Medical University, Beijing, China Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China.
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Wang
School of Public Health, Capital Medical University, Beijing, China Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China.
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Gao
School of Public Health, Capital Medical University, Beijing, China Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China.
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Niu
School of Public Health, Capital Medical University, Beijing, China Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China.
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Chen
School of Public Health, Capital Medical University, Beijing, China Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China tian_lin@163.com.
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Tian
D000818:Animals; D055419:Bone Morphogenetic Protein 7 / Q000008:administration & dosage / Q000494:pharmacology*; D045744:Cell Line, Tumor; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects*; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D008168:Lung / Q000187:drug effects / Q000473:pathology; D008297:Male; D011658:Pulmonary Fibrosis / Q000139:chemically induced*; D051381:Rats; D017208:Rats, Wistar; D011994:Recombinant Proteins; D012822:Silicon Dioxide / Q000633:toxicity*; D012829:Silicosis / Q000517:prevention & control*; D051900:Smad3 Protein / Q000235:genetics / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism; D014746:Vimentin / Q000235:genetics / Q000378:metabolism
D055419:Bone Morphogenetic Protein 7; D011994:Recombinant Proteins; D051900:Smad3 Protein; C497787:Smad3 protein, rat; D053773:Transforming Growth Factor beta1; D014746:Vimentin; D012822:Silicon Dioxide
Bone morphogenetic protein-7; epithelial–mesenchymal transition; pulmonary fibrosis; silica