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  • Title: LncRNA MEG3 mediates nickel oxide nanoparticles-induced pulmonary fibrosis via suppressing TGF-β1 expression and epithelial-mesenchymal transition process.
    Author: Zhan H, Chang X, Wang X, Yang M, Gao Q, Liu H, Li C, Li S, Sun Y.
    Journal: Environ Toxicol; 2021 Jun; 36(6):1099-1110. PubMed ID: 33547861.
    Abstract:
    Nickel oxide nanoparticles (NiO NPs) causes pulmonary fibrosis via activating transforming growth factor-β1 (TGF-β1) in rats, but its upstream regulatory mechanisms are unknown. This study aimed to explore the role of long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) in NiO NPs-induced collagen deposition. Male Wistar rats were intratracheally instilled with NiO NPs (0.015, 0.06, and 0.24 mg/kg b.w.) twice a week for 9 weeks. Human lung adenocarcinoma epithelial cells (A549 cells) were cultured with NiO NPs (25, 50, and 100 μg/ml) to establish collagen deposition model. We discovered that NiO NPs-induced rat pulmonary fibrosis was accompanied by the epithelial-mesenchymal transition (EMT) occurrence and MEG3 down-regulation in rat lung tissues. In cell collagen deposition model, NiO NPs also evoked EMT and decreased MEG3 expression in a dose-dependent manner in A549 cells. By overexpressing MEG3 in A549 cells, we found that MEG3 inhibited the level of TGF-β1, EMT process and collagen formation. Moreover, our data showed that SB431542 (TGF-β1 inhibitor) had an inhibitory effect on NiO NPs-induced EMT and collagen formation. Our results indicated that MEG3 inhibited NiO NPs-induced collagen deposition by regulating TGF-β1-mediated EMT process, which may provide some clues for insighting into the mechanisms of NiO NPs-induced pulmonary fibrosis.
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