AI Article Synopsis
- The epithelial-mesenchymal transition (EMT) involves the transformation of epithelial cells into mesenchymal cells, contributing to lung fibrosis, and is significantly influenced by the TGF-β/SMAD signaling pathway.
- Research showed that silica exposure leads to EMT in A549 cells, which was inhibited by the compound SB431542, indicating its regulatory role in improving fibrotic responses by manipulating protein expressions like Vimentin and E-cadherin.
- Additionally, blocking BMP/SMAD signaling exacerbated EMT, suggesting a complex interaction between TGF-β/SMAD and BMP/SMAD pathways during silica-induced EMT in lung cells.
Article Abstract
The epithelial-mesenchymal transition (EMT) is a phenotype transdifferentiation of epithelial into mesenchymal cells and contributes to pulmonary fibrotic disease. SMAD-dependent pathway has been reported to play a key role in the multiple fibrotic diseases. We hypothesized that TGF-β/SMAD signaling could cross-interact with BMP/SMAD signaling pathways in silica-induced EMT in A549 cells. We investigated that the ability of silica-induced EMT in A549 cells, and this process was significantly inhibited by SB431542 through up-regulation of Vimentin, α-SMA and collagen type I expression and down-regulation of E-cadherin expression. Whereas BMP/SMAD inhibition using LDN193189 enhanced EMT. In addition, we also demonstrated that SB431542 could enhance BMP/SMAD signaling pathways in silica-induced EMT and vice versa. Therefore, our study provides evidence that the TGF-β/SMAD pathway was a crucial regulator in silica-induced EMT and that SB431542 could prevent the EMT. More importantly, we have identified that the interplay of TGF-β/SMAD and BMP/SMAD pathways in silica-induced EMT in A549 cells.
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| http://dx.doi.org/10.1080/15376516.2017.1407978 | DOI Listing |
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