【摘 要】
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Objective: To investigate the anti-fibrotic effects and possible mechanisms of bone morphogenetic protein-7 (BMP-7) on silica induced fibrosis in RLE-6TN cells, and compare the preventive treatment of
【机 构】
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Department of Occupational and Environmental Health, School of Public Health, Capital Medical Univer
【出 处】
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首都医科大学公共卫生学院第四届研究生学术论坛
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Objective: To investigate the anti-fibrotic effects and possible mechanisms of bone morphogenetic protein-7 (BMP-7) on silica induced fibrosis in RLE-6TN cells, and compare the preventive treatment of experimental silicosis with BMP-7 with therapeutic treatment of silicosis in vitro models.Methods: RLE-6TN cells were incubated with the supernatant of RAW264.7,treated by 50 μg/ml silica in either presence or absence of BMP-7 in different phases.Morphological changes and the cellular wound-healing assays were used to evaluate the process of EMT.By using Western Blotting, the epithelial marker E-cadherin (E-cad), and the mesenchymal markers Vimentin (Vim), Snail, and fibronectin (FN) were detected as well as the Smad signaling pathway proteins, including phosphorylated Smad1/5(P-Smad1/5), phosphorylated Smad2/3(P-Smad2/3), and non-phosphorylated Smad1, Smad8, and Smad2.The progress of fibrosis was assessed by the content of hydroxyproline (Hyp) and collagen Ⅰ and Ⅲprotein levels.In addition, MTT assay was used to explore the toxic effects of silica as well as BMP-7.Results:The EMT model of RLE-6TN cells was established successfully, the cells had a fibroblast-like morphology with increasing migration activity.The expressions of Vim, Snail, FN, collagen Ⅰ and collagen Ⅲ were up-regulated with the increase of silica concentration.BMP-7 could attenuate the decrease of P-Smad1/5 and the increase of P-Smad2/3, collagen Ⅰ, collagen Ⅲ, and FN via Smad signaling pathway.BMP-7 inhibited the mesenchymal-like responses in RLE-6TN cells, including cell migration, expression of fibrosis markers, and secretion of Hyp.Furthermore, the anti-fibrotic effects in the prevention group were more effective than treatment group.Conclusion: The restoration of BMP signaling with BMP-7 is associated with inhibiting silica-induced fibrosis through the mechanisms of activated BMP-7/Smad and suppressed TGF-β/Smad pathways.Preventive treatment of pulmonary fibrosis progression with BMP-7 may expect to be the optimized strategy than therapeutic therapy of fibrosis.
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