Journal
JOURNAL OF HAZARDOUS MATERIALS
Volume 430, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.jhazmat.2022.128485
Keywords
Newly-emerging hazardous material; Nanoplastics; Toxicologic mechanism; Epithelial-to-mesenchymal transition
Categories
Funding
- National Natural Science Foundation of China [41877503, 31670516]
- International Science & Technology Innovation Program of Chinese Academy of Agricultural Sciences [CAAS-ZDRW202110]
- Science and Technology Agency Livelihood Program of Liaoning Province of China [2021JH2/10300075]
- Liaoning Revitalization Talents Program [XLYC1807226]
- Shenyang HighLevel Innovative Talents Program [RC190060]
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This study reveals that polystyrene nanoplastics (PS-NPs) can increase the risk of lung fibrosis by inducing epithelial-to-mesenchymal transition (EMT) in alveolar epithelial cells. This process may be mediated by the up-regulation of reactive oxygen species (ROS) and NADPH oxidase 4 (NOX4), as well as mitochondrial dysfunction, among other mechanisms. Furthermore, smaller PS-NPs with a positive surface charge show stronger effects and the involvement of NOX4 is essential in this process.
As a newly emerging hazardous material, airborne nanoplastics are easily inhaled and accumulated in human and animal alveoli. We previously found that polystyrene nanoplastics (PS-NPs) induced apoptosis and inflammation of human alveolar epithelial A549 cells, implying they increase the risk of pulmonary fibrosis. In this study, we investigated whether PS-NPs induce epithelial-to-mesenchymal transition (EMT), the prelude to lung fibrosis, in A549 cells. A549 cells treated with PS-NPs of different sizes and surface charges exhibited increased migration and EMT markers accompanied with up-regulation of reactive oxygen species (ROS) and NADPH oxidase 4 (NOX4), an ROS generator located in the mitochondria and endoplasmic reticulum (ER). Moreover, PS-NPs caused mitochondrial dysfunction as demonstrated by membrane potential changes and impaired cellular energy metabolism. PS-NPs also activated ER stress as indicated by the up-regulated ER stress markers. As expected, smaller PS-NPs with a positive surface charge had stronger effects. Furthermore, the effects of PS-NPs on A549 cells were reversed by NOX4 gene knock-down, which verified the involvement of NOX4. Our results suggest that PS-NPs induce EMT in A549 cells through multiple mechanisms, and NOX4 is a key mediator in this process. Our findings contribute to understanding the toxicological mechanisms of nanoplastics on the respiratory system.
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