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

Abstract 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 show...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Jun Zhao, Jinding Pu, Binwei Hao, Lingmei Huang, Jinglong Chen, Wei Hong, Yumin Zhou, Bing Li, Pixin Ran
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2020
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/cc5abfdab36d447bac86fdaef41f8a1a
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:cc5abfdab36d447bac86fdaef41f8a1a
record_format	dspace
spelling	oai:doaj.org-article:cc5abfdab36d447bac86fdaef41f8a1a2021-12-02T15:32:59ZLncRNA RP11-86H7.1 promotes airway inflammation induced by TRAPM2.5 by acting as a ceRNA of miRNA-9-5p to regulate NFKB1 in HBECS10.1038/s41598-020-68327-12045-2322https://doaj.org/article/cc5abfdab36d447bac86fdaef41f8a1a2020-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-68327-1https://doaj.org/toc/2045-2322Abstract 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.Jun ZhaoJinding PuBinwei HaoLingmei HuangJinglong ChenWei HongYumin ZhouBing LiPixin RanNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 10, Iss 1, Pp 1-14 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Jun Zhao Jinding Pu Binwei Hao Lingmei Huang Jinglong Chen Wei Hong Yumin Zhou Bing Li Pixin Ran 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
description	Abstract 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.
format	article
author	Jun Zhao Jinding Pu Binwei Hao Lingmei Huang Jinglong Chen Wei Hong Yumin Zhou Bing Li Pixin Ran
author_facet	Jun Zhao Jinding Pu Binwei Hao Lingmei Huang Jinglong Chen Wei Hong Yumin Zhou Bing Li Pixin Ran
author_sort	Jun Zhao
title	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
title_short	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
title_full	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
title_fullStr	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
title_full_unstemmed	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
title_sort	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
publisher	Nature Portfolio
publishDate	2020
url	https://doaj.org/article/cc5abfdab36d447bac86fdaef41f8a1a
work_keys_str_mv	AT junzhao lncrnarp1186h71promotesairwayinflammationinducedbytrapm25byactingasacernaofmirna95ptoregulatenfkb1inhbecs AT jindingpu lncrnarp1186h71promotesairwayinflammationinducedbytrapm25byactingasacernaofmirna95ptoregulatenfkb1inhbecs AT binweihao lncrnarp1186h71promotesairwayinflammationinducedbytrapm25byactingasacernaofmirna95ptoregulatenfkb1inhbecs AT lingmeihuang lncrnarp1186h71promotesairwayinflammationinducedbytrapm25byactingasacernaofmirna95ptoregulatenfkb1inhbecs AT jinglongchen lncrnarp1186h71promotesairwayinflammationinducedbytrapm25byactingasacernaofmirna95ptoregulatenfkb1inhbecs AT weihong lncrnarp1186h71promotesairwayinflammationinducedbytrapm25byactingasacernaofmirna95ptoregulatenfkb1inhbecs AT yuminzhou lncrnarp1186h71promotesairwayinflammationinducedbytrapm25byactingasacernaofmirna95ptoregulatenfkb1inhbecs AT bingli lncrnarp1186h71promotesairwayinflammationinducedbytrapm25byactingasacernaofmirna95ptoregulatenfkb1inhbecs AT pixinran lncrnarp1186h71promotesairwayinflammationinducedbytrapm25byactingasacernaofmirna95ptoregulatenfkb1inhbecs
_version_	1718387170080718848

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

Ejemplares similares