Mechanism of Interaction between hsa_circ_0002854 and MAPK1 Protein in PM2.5-Induced Apoptosis of Human Bronchial Epithelial Cells

• Published in: Toxics (Basel) Vol. 11; no. 11; p. 906
• Main Authors: Hong, Jinchang, Tan, Yi, Wang, Yuyu, Wang, Hongjie, Li, Caixia, Jin, Wenjia, Wu, Yi, Ni, Dechun, Peng, Xiaowu
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 01.11.2023
• Subjects: Air pollution; Apoptosis; Asthma; atmospheric fine particles; Biology; Cell proliferation; Cells; Chronic obstructive pulmonary disease; Circular RNA; Concentration gradient; Epithelial cells; Epithelium; Exposure; Flow cytometry; Functional analysis; Gene therapy; Health risks; human bronchial epithelial cells; Lung cancer; Lung diseases; MAPK1; Mortality; Nitrogen dioxide; Outdoor air quality; Particulate matter; Phosphorylation; Proteins; Pulmonary fibrosis; Reagents; Respiratory diseases; Respiratory system; United States > US; China
• ISSN: 2305-6304; 2305-6304
• DOI: 10.3390/toxics11110906

Fine particulate matter (PM2.5) pollution increases the risk of respiratory diseases and death, and apoptosis is an important factor in the occurrence of respiratory diseases caused by PM2.5 exposure. In addition, circular RNAs (circRNAs) can interact with proteins and widely participate in physiological and pathological processes in the body. The aim of this study was to investigate the mechanism of circRNA and protein interaction on PM2.5-induced apoptosis of human bronchial epithelial cells (16HBE) in vitro. In this study, we exposed human bronchial epithelial cells to a PM2.5 suspension with different concentration gradients for 24 h. The results showed that apoptosis of 16HBE cells after PM2.5 treatment was accompanied by cell proliferation. After exposure of PM2.5 to 16HBE cells, circRNAs related to apoptosis were abnormally expressed. We further found that the expression of hsa_circ_0002854 increased with the increase in exposure concentration. Functional analysis showed that knocking down the expression of hsa_circ_0002854 could inhibit apoptosis induced by PM2.5 exposure. We then found that hsa_circ_0002854 could interact with MAPK1 protein and inhibit MAPK1 phosphorylation, thus promoting apoptosis. Our results suggest that hsa_circ_0002854 can promote 16HBE apoptosis due to PM2.5 exposure, which may provide a gene therapy target and scientific basis for PM2.5-induced respiratory diseases.