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首页> 外文期刊>The Journal of toxicological sciences >Involvement of epithelial-mesenchymal transition in methotrexate-induced pulmonary fibrosis
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Involvement of epithelial-mesenchymal transition in methotrexate-induced pulmonary fibrosis

机译：上皮-间质转化参与甲氨蝶呤诱导的肺纤维化

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Epithelial-mesenchymal transition (EMT) plays a pivotal event in the development of pulmonary fibrosis. We have previously reported that methotrexate (MTX)-induced alveolar epithelial cell injury followed by pulmonary fibrosis as a result of the recruitment and proliferation of myofibroblasts. However, there is no data concerning whether EMT occurs in MTX-induced pulmonary fibrosis. In the present study, therefore, we investigated the expression of EMT markers such as E-cadherin, α-SMA, and vimentin by immunofluorescence analysis in mouse lung tissues after administration of MTX. We found that vimentin and α-SMA-positive cells of the MTX-induced pulmonary fibrosis were increased; on the other hand, E-cadherin was decreased, indicating that epithelial cells act as the main source of mesenchymal expansion. These results exhibited the down-regulation of E-cadherin expression and the up-regulation of α-smooth muscle actin (α-SMA) in primary mouse alveolar epithelial cells (MAECs) and A549 cell lines. Additionally, MTX-induced A549 cells exhibited an EMT-like phenotype accompanied by the elevation of the expression of interleukin-6 (IL-6) and transforming growth factor (TGF)-β1, as well as an enhancement of migration. All of these findings suggest that MTX-induced pulmonary fibrosis occurs via EMT.
机译：上皮-间质转化（EMT）在肺纤维化发展中起关键作用。我们以前曾报道过，由于肌成纤维细胞的募集和增殖，甲氨蝶呤（MTX）引起的肺泡上皮细胞损伤继之以肺纤维化。但是，没有关于在MTX诱导的肺纤维化中是否发生EMT的数据。因此，在本研究中，我们通过免疫荧光分析研究了MTX给药后小鼠肺组织中EMT标记物（如E-钙黏着蛋白，α-SMA和波形蛋白）的表达。我们发现，MTX诱导的肺纤维化的波形蛋白和α-SMA阳性细胞增加;另一方面，E-钙黏着蛋白减少，表明上皮细胞是间充质扩张的主要来源。这些结果显示原代小鼠肺泡上皮细胞（MAECs）和A549细胞系中E-钙黏着蛋白表达下调和α-平滑肌肌动蛋白（α-SMA）上调。此外，MTX诱导的A549细胞表现出EMT样表型，并伴有白介素6（IL-6）和转化生长因子（TGF）-β1表达的升高，以及迁移的增强。所有这些发现表明，MTX诱导的肺纤维化是通过EMT发生的。

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