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Bone morphogenetic protein-7 prevented epithelial-mesenchymal transition in RLE-6TN cells

机译:骨形态发生蛋白7阻止RLE-6TN细胞上皮-间质转化

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摘要

Bone morphogenetic protein-7 (BMP-7) plays an important role in the epithelial-mesenchymal transition (EMT) process, and has been identified as the most potent factor that can promote mesenchymal-epithelial transition (MET) and reduce organ fibrosis. Here we examined the important role of BMP-7 in silica-induced EMT and investigated the relationship between BMP-7 and the balance of EMT/MET. We found that silica induced EMT and decreased the expression of BMP-7 in vivo and in vitro, while silica activated the p38 MAPK/transcription factor signaling pathway in RLE-6TN cells. Lentivirus mediated transfection was used to stably upregulate the expression of BMP-7. Exogenous BMP-7 brought on MET exceeded silica-induced EMT and restrained the p38 MAPK/transcription factor signaling pathway in RLE-6TN cells. Our results revealed that BMP-7 promoted MET above EMT induced by silica associated with inhibition of the p38 MAPK/transcription factor signaling pathway, and BMP-7 was a potential target for treatment of silicosis fibrosis.
机译:骨形态发生蛋白7(BMP-7)在上皮-间质转化(EMT)过程中起着重要作用,并且已被确定为可以促进间质-上皮转化(MET)和减少器官纤维化的最有效因子。在这里,我们研究了BMP-7在二氧化硅诱导的EMT中的重要作用,并研究了BMP-7与EMT / MET平衡之间的关系。我们发现,二氧化硅可诱导EMT并在体内和体外降低BMP-7的表达,而二氧化硅可激活RLE-6TN细胞中的p38 MAPK /转录因子信号通路。慢病毒介导的转染用于稳定上调BMP-7的表达。 MET上的外源BMP-7超过了二氧化硅诱导的EMT,并限制了RLE-6TN细胞中的p38 MAPK /转录因子信号通路。我们的研究结果表明,BMP-7促进了MET诱导的EMT高于由二氧化硅诱导的EMT,这与p38 MAPK /转录因子信号通路的抑制有关,而BMP-7是治疗矽肺纤维化的潜在靶标。

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