Volume 49 Number 3

Circular RNA ARF3 attenuates PM_2.5-induced inflammatory response in human bronchial epithelial cells by regulating microRNA-509-3p and chromodomain helicase DNA binding protein 9

Zhu Zhou, YiMei Wang, Xiang Huang, LiWen Zhang, Di Wu, Yi Ren, Fei Lu, XiKun Gao^*

 
ABSTRACT:      The present study deciphered the molecular mechanisms by which circARF3 attenuates particulate matter 2.5 (PM2.5)-induced bronchial epithelial cell damage. Bronchial epithelial injury was modeled by PM2.5 exposure. To regulate circARF3, microRNA-509-3p (miR-509-3p) and Chromodomain Helicase DNA Binding Protein 9 (CHD9), plasmid transfection and oligonucleotide techniques were used. Cell viability was quantified by Cell Counting Kit-8 assay. Apoptosis rate was determined by flow cytometry, while apoptotic genes were assessed by quantitative real-time polymerasechainreaction. Reactiveoxygenlevelsweremeasuredusinga2?,7?-dichlorofluoresceindiacetatefluorescent probe. Levels of the inflammatory cytokines were assessed by enzyme-linked immunosorbent assay, and CHD9, Toll Like Receptor 4, and phosphorylated nuclear factor-kappa B subunit p65 were measured by Western blotting analysis. Targeted interactions between miR-509-3p, circARF3 and CHD9 were verified using dual luciferase reporter and RNA immunoprecipitation assays. Exposure to PM2.5 decreased bronchial epithelial cell viability, increased apoptosis, and elevated ROS while activating the TLR4/NF-?B pathway. CircARF3 overexpression or knockdown inhibited and promoted PM2.5-induced injury, respectively. Overexpressing miR-509-3p exacerbated PM2.5-induced injury, whereas overexpressing CHD9 showed the opposite effect. CircARF3 competitively bound miR-509-3p to mediate CHD9 expression. CircARF3 attenuates PM2.5-induced damage to bronchial epithelial cells by regulating miR-509-3p and promoting CHD9 expression.

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* Corresponding author, E-mail: cssgaoxikun@163.com

Received 19 Apr 2023, Accepted 28 Nov 2024