Loss of E-cadherin due to road dust PM2.5 activates the EGFR in human pharyngeal epithelial cells
Journal
Environmental Science and Pollution Research
Date Issued
2021
Author(s)
Tung N.T
Abstract
Exposure to road dust particulate matter (PM) causes adverse health impacts on the human airway. However, the effects of road dust on the upper airway epithelium in humans remain unclear. We investigated the involvement of the epidermal growth factor receptor (EGFR) after PM with an aerodynamic diameter of < 2.5 μm (PM2.5)-induced E-cadherin disruption of human pharyngeal epithelial cells. First, we collected road dust PM2.5 from 10 Chinese cities, including Wuhan, Nanjing, Shanghai, Guangzhou, Chengdu, Beijing, Lanzhou, Tianjin, Harbin, and Xi’an. Human pharyngeal FaDu cells were exposed to road dust PM2.5 at 50 μg/mL for 24 h, cytotoxicity (cell viability and lactate dehydrogenase (LDH)) was assessed, and expressions of the proinflammatory interleukin (IL)-6 and high-mobility group box 1 (HMGB1) protein, receptor for advanced glycation end products (RAGE), occludin, E-cadherin, EGFR, and phosphorylated (p)-EGFR were determined. The E-cadherin gene was then knocked down to investigate EGFR activation in FaDu cells. Exposure to road dust PM2.5 resulted in a decrease in cell viability and increases in LDH and IL-6. Our data suggested that PM2.5 could decrease expressions of occludin and E-cadherin and increase expressions of EGFR and p-EGFR, which was confirmed by E-cadherin-knockdown. Our results showed a negative association between the alterations in E-cadherin and total elemental components in correlation analysis, especially S, Cl, K, Ti, Mn, Fe, Cu, Zn, and Pb. Exposure to metals in PM2.5 from road dust may lead to loss of the barrier function of the upper airway epithelium and activation of the EGFR. Our study showed the adverse effects of road dust PM2.5 on pharyngeal epithelial cells of the human upper airway. ? 2021, The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
Subjects
Air pollution; Allergy; Chemical; Metal; Particulate matter; Upper airway
Other Subjects
cell; cell component; detection method; dust; gene expression; particulate matter; urban area; cadherin; EGFR protein, human; epidermal growth factor receptor; air pollutant; analysis; China; city; dust; environmental monitoring; epithelium cell; genetics; human; particulate matter; toxicity; Air Pollutants; Cadherins; China; Cities; Dust; Environmental Monitoring; Epithelial Cells; ErbB Receptors; Humans; Particulate Matter
Type
journal article