Abstract
Our previous study demonstrated that nano nickel oxide (NiO) induce pulmonary fibrosis in rats and collagen excessive formation in A549 cells, which mechanism was related with the increasing transforming growth factor β1 (TGF-β1) secretion. However, it remains unclear understanding the role of TGF-β1 in collagen excessive formation. Here, we found nano NiO could directly promote epithelial-mesenchymal transition (EMT) via the TGF-β1/Smads pathway in A549 cells. First, cytotoxicity induced by nano NiO has a dose- and time-dependent manner according to methylthiaozol tetrazolium assay. Second, nano NiO led to the increased contents of type I collagen (Col-I), TGF-β1, p-Smad2, p-Smad3, alpha-smooth muscle actin (α-SMA), vimentin, and fibronectin, indicating Smads pathway activation and EMT occurence. Third, to verify whether TGF-β1 activated Smads signaling pathway and EMT occurence, A549 cells were exposed to nano NiO and TGF-β1 inhibitors (10 μM SB431542). The results showed that TGF-β1 inhibitors alleviated the nano NiO-induced cytotoxicity and Col-I excessive formation. Meanwhile, TGF-β1 inhibitors reversed the proteins expression trends of Col-I, p-Smad2, p-Smad3, α-SMA, vimentin, fibronectin, and E-cadherin. These observations suggested that EMT occurrence via TGF-β1/Smads pathway might play an important role in the collagen excessive formation induced by nano NiO in A549 cells.
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