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Bone morphogenetic protein 7 attenuates epithelial-mesenchymal transition induced by silica.
Yang, G; Zhu, Z; Wang, Y; Gao, A; Niu, P; Chen, L; Tian, L.
Affiliation
  • Yang G; 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.
  • Zhu Z; 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.
  • Wang Y; School of Public Health, Capital Medical University, Beijing, China Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China.
  • Gao A; School of Public Health, Capital Medical University, Beijing, China Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China.
  • Niu P; School of Public Health, Capital Medical University, Beijing, China Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China.
  • Chen L; School of Public Health, Capital Medical University, Beijing, China Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China.
  • Tian L; School of Public Health, Capital Medical University, Beijing, China Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China tian_lin@163.com.
Hum Exp Toxicol ; 35(1): 69-77, 2016 Jan.
Article in En | MEDLINE | ID: mdl-25733726
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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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Pulmonary Fibrosis / Silicosis / Silicon Dioxide / Bone Morphogenetic Protein 7 / Epithelial-Mesenchymal Transition Type of study: Prognostic_studies Limits: Animals / Humans / Male Language: En Journal: Hum Exp Toxicol Journal subject: TOXICOLOGIA Year: 2016 Document type: Article
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Pulmonary Fibrosis / Silicosis / Silicon Dioxide / Bone Morphogenetic Protein 7 / Epithelial-Mesenchymal Transition Type of study: Prognostic_studies Limits: Animals / Humans / Male Language: En Journal: Hum Exp Toxicol Journal subject: TOXICOLOGIA Year: 2016 Document type: Article