CircRNA104250 and lncRNAuc001.dgp.1 promote the PM2.5-induced inflammatory response by co-targeting miR-3607-5p in BEAS-2B cells
2020
Li, Xin | Jia, Yangyang | Nan, Aruo | Zhang, Nan | Zhou, Hanyu | Chen, Lijian | Pan, Xiujiao | Qiu, Miaoyun | Zhu, Jialu | Zhang, Han | Ling, Yihui | Jiang, Yiguo
Long-term exposure to particulate matter 2.5 (PM₂.₅) is closely related to the occurrence and development of airway inflammation. Exploration of the role of PM₂.₅ in inflammation is the first step towards clarifying the harmful effects of particulate pollution. However, the molecular mechanisms underlying PM₂.₅-induced airway inflammation are yet to be fully established. In this study, we focused on the specific roles of non-coding RNAs (ncRNAs) in PM₂.₅-induced airway inflammation. In a human bronchial epithelial cell line, BEAS-2B, PM₂.₅ at a concentration of 75 μg/mL induced the inflammatory response. Microarray and quantitative real-time polymerase chain reaction (qRT-PCR) analyses revealed significant upregulation of circRNA104250 and lncRNAuc001.dgp.1 during the PM₂.₅-induced inflammatory response in this cell line. Data from functional analyses further showed that both molecules promote an inflammatory response. CircRNA104250 and lncRNAuc001.dgp.1 target miR-3607-5p and affect expression of interleukin 1 receptor 1 (IL1R1), which influences the nuclear factor κB (NF-κB) signaling pathway. In summary, we have uncovered an underlying mechanism of airway inflammation by PM₂.₅ involving regulation of ncRNA for the first time, which provides further insights into the toxicological effects of PM₂.₅.
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