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  • Title: TGF-β1 mediated MAPK signaling pathway promotes collagen formation induced by Nano NiO in A549 cells.
    Author: Tian M, Chang X, Zhang Q, Li C, Li S, Sun Y.
    Journal: Environ Toxicol; 2019 Jun; 34(6):719-727. PubMed ID: 30810263.
    Abstract:
    Nickel oxide nanoparticles (Nano NiO) could induce pulmonary fibrosis, however, the mechanisms are still unknown. The aim of the present study was to explore the roles of transforming growth factor-β1 (TGF-β1), mitogen-activated protein kinase (MAPK) pathway and MMPs/TIMPs balance in Nano NiO-induced pulmonary fibrosis. For that purpose, we first established Nano NiO-induced human lung adenocarcinoma epithelial cells (A549 cells) model of collagen excessive formation through detecting the levels of hydroxyproline (Hyp) and type I collagen (Col-I). Then the protein levels of TGF-β1, MAPKs, and MMPs/TIMPs were assessed by Western blot. The results showed that Nano NiO resulted in the increased contents of Hyp, Col-I, and TGF-β1, the MAPK pathway activation and MMPs/TIMPs imbalance with a dose-dependent manner. In addition, to investigate whether TGF-β1 mediated MAPK signaling pathway, A549 cells were treated by 100 μg/mL Nano NiO combined with TGF-β1, p38 MAPK, and ERK1/2 inhibitors (10 μM SB431542, 10 μM SB203580, and 10 μM U0126), respectively. We found that MAPK signal pathway was suppressed by TGF-β1 inhibitor. Meanwhile, the increased contents of Hyp and Col-I, and MMPs/TIMPs imbalance were alleviated by the p38 MAPK and ERK1/2 inhibitors, respectively. These findings indicated that the MAPK pathway and MMPs/TIMPs imbalance were involved in collagen excessive formation induced by Nano NiO.
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