Circular RNA ARF3 attenuates PM2.5-induced inflammatory response in human bronchial epithelial cells by regulating microRNA-509-3p and chromodomain helicase DNA binding protein 9

Abstract

The present study deciphered the molecular mechanisms by which circARF3 attenuates particulate matter 2.5 (PM 2.5 )-induced bronchial epithelial cell damage.Bronchial epithelial injury was modeled by PM 2.5 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 polymerase chain reaction.Reactive oxygen levels were measured using a 2 ,7 -dichlorofluorescein diacetate fluorescent 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 PM 2.5 decreased bronchial epithelial cell viability, increased apoptosis, and elevated ROS while activating the TLR4/NF-B pathway.CircARF3 overexpression or knockdown inhibited and promoted PM 2.5 -induced injury, respectively.Overexpressing miR-509-3p exacerbated PM 2.5 -induced injury, whereas overexpressing CHD9 showed the opposite effect.CircARF3 competitively bound miR-509-3p to mediate CHD9 expression.CircARF3 attenuates PM 2.5 -induced damage to bronchial epithelial cells by regulating miR-509-3p and promoting CHD9 expression.