LncRNA RP11-86H7.1 promotes airway inflammation induced by TRAPM2.5 by acting as a ceRNA of miRNA-9-5p to regulate NFKB1 in HBECS

• Published in: Scientific reports Vol. 10; no. 1; pp. 11587 - 14
• Main Authors: Zhao, Jun, Pu, Jinding, Hao, Binwei, Huang, Lingmei, Chen, Jinglong, Hong, Wei, Zhou, Yumin, Li, Bing, Ran, Pixin
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 14.07.2020; Nature Publishing Group; Nature Portfolio
• Subjects: 631/337; 692/4017; 692/420; 692/53; 692/699; 704/172; Air pollution; Bronchi - drug effects; Bronchi - pathology; Chronic obstructive pulmonary disease; Epithelial cells; Epithelial Cells - drug effects; Gases; Gene Expression Regulation - drug effects; Humanities and Social Sciences; Humans; Inflammation; Inflammation - chemically induced; Inflammation - genetics; Inflammation - pathology; Lung - drug effects; Lung - pathology; Lung diseases; MicroRNAs - genetics; miRNA; multidisciplinary; NF-kappa B p50 Subunit - genetics; NF-κB protein; Obstructive lung disease; Outdoor air quality; Particulate matter; Particulate Matter - toxicity; Pulmonary Disease, Chronic Obstructive - chemically induced; Pulmonary Disease, Chronic Obstructive - genetics; Pulmonary Disease, Chronic Obstructive - pathology; Respiratory tract; Respiratory tract diseases; RNA, Long Noncoding - genetics; Science; Science (multidisciplinary); Signal transduction; Therapeutic applications; Vehicle Emissions - toxicity
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-020-68327-1

Traffic-related air pollution particulate matter 2.5 (TRAPM2.5), is involved in chronic obstructive pulmonary disease (COPD), which is characterized by airway inflammation. Specifically, these harmful particles or gases can increase chronic airway inflammation. Some recent studies have shown that lncRNAs are closely related to COPD and participate in the regulation of airway inflammation. However, the precise mechanisms remain unknown. In the present study, we investigated the effect of TRAPM2.5 on airway inflammation in human bronchial epithelial cells (HBECs) and the underlying mechanisms mediated by a lncRNA. After exposure to TRAPM2.5, the novel lncRNA RP11-86H7.1 was markedly upregulated in HBECs. Functional assays indicated that the lncRNA RP11-86H7.1 was required for the TRAPM2.5-induced expression of inflammatory factors in HBECs. A mechanistic study demonstrated that lncRNA RP11-86H7.1 might participate in TRAPM2.5-induced inflammatory responses by activating the NF-κB signaling pathway. Moreover, the lncRNA RP11-86H7.1 can promote the inflammatory response by acting as a competing endogenous RNA of miR-9-5p, reversing the inhibitory effect of its target gene NFKB1, and sustaining NF-κB activation. In summary, our study elucidates the pro-inflammatory roles of the lncRNA RP11-86H7.1–miR-9-5p–NFKB1 regulatory network in airway inflammation induced by TRAPM2.5 and indicates that the components of this network might serve as novel diagnostic biomarkers and potential therapeutic targets.