Diesel exhaust particle exposure accelerates oxidative DNA damage and cytotoxicity in normal human bronchial epithelial cells through PD-L1
- Authors
- Kwon, Minji; Jung, Jiwoo; Park, Hee Sun; Kim, Na Hui; Lee, Jiwoo; Park, Jayeon; Kim, Youjin; Shin, Seokwon; Lee, Byung Soo; Cheong, Ye Hwang; Youn, Hyung-Sun; Kim, Sung Roul; Park, Sin-Aye
- Issue Date
- Jan-2023
- Publisher
- Pergamon Press Ltd.
- Keywords
- Diesel exhaust particles; Programmed death-ligand 1; Reactive oxygen species; DNA damage; Heme oxygenase-1; Human bronchial epithelial cells
- Citation
- Environmental Pollution, v.317
- Journal Title
- Environmental Pollution
- Volume
- 317
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/22262
- DOI
- 10.1016/j.envpol.2022.120705
- ISSN
- 0269-7491
1873-6424
- Abstract
- Diesel exhaust particles (DEPs) are a major cause of cancer progression as well as a variety of acute and chronic diseases. It is well-known that programmed death-ligand 1 (PD-L1) is an immune checkpoint molecule that can induce immune escape in tumor cells. However, the function of PD-L1 in bronchial epithelial cells or how PD-L1 relates to cellular oxidation under DEPs-mediated oxidative stress is not well known. In this study, we investigated how PD-L1 affected DEPs-induced oxidative stress and cytotoxicity in human bronchial epithelial (HBE) cells, Beas-2B. DEPs not only induced intracellular reactive oxygen species (ROS) production, but also increased PD-L1 expression in HBE cells. Beas-2B cells overexpressing PD-L1 showed higher levels of ROS production, DNA damage, and apoptosis after DEPs treatment compared to control cells. In particular, the expression of an antioxidant enzyme heme-oxygenase-1 (HO-1) and nuclear translocation and transcriptional activity of Nrf2, a major regulator of HO-1, were lower in Beas-2B overexpressing PD-L1 cells than in control cells. DEPs-induced ROS generation, DNA damage and apoptosis in Beas-2B cells overexpressing PD-L1 were significantly restored by overexpressing HO-1. Collectively, our results suggest that DEPs can increase the expression of PD-L1 in HBE cells and that overexpressing PD-L1 might eventually promote DEPs-induced oxidative DNA damage and apoptosis.
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- Appears in
Collections - College of Natural Sciences > Department of Environmental Health Science > 1. Journal Articles
- College of Medical Sciences > Department of Biomedical Laboratory Science > 1. Journal Articles
- College of Engineering > Department of Information and Communication Engineering > 1. Journal Articles
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