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MiR-218 Inhibits CSE-Induced Apoptosis and Inflammation in BEAS-2B by Targeting BRD4.

Abstract：

Background:Chronic obstructive pulmonary disease (COPD) is an age-related disease, and its incidence rate is increasing every year. MicroRNAs (miRNAs) play critical roles in the COPD process and function as key biomarkers or potential therapeutic targets for patients with COPD. However, the potential roles and functional effects of miR-218 in COPD remain undefined. Methods:The expression levels of miR-218 and bromodomain protein 4 (BRD4) were assessed by real-time quantitative polymerase chain reaction (RT-qPCR) or Western blot, respectively. In addition, a COPD cell model was established using cigarette smoke extract (CSE) in bronchial epithelial cell line (BEAS-2B). Enzyme-linked immunosorbent assay (ELISA) kit was applied to measure the concentrations of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-8 (IL-8) in cell supernatants of BEAS-2B cells. Moreover, cell apoptosis was examined by flow cytometry assay. The association relationship between miR-218 and BRD4 was confirmed by dual-luciferase reporter and RNA immunoprecipitation assay. Results:MiR-218 was downregulated in COPD and CSE-induced BEAS-2B cells, and it was positively correlated with forced expiratory volume in 1 second (FEV1) % in COPD patients. Mechanically, overexpression of miR-218 or knockdown of BRD4 mitigated apoptosis and inflammation in BEAS-2B cells induced by CSE. Additionally, overexpression of BRD4 weakened the miR-218-mediated effects on CSE-induced BEAS-2B cells. Conclusion:Overexpression of miR-218 inhibited CSE-induced apoptosis and inflammation in BEAS-2B cells by targeting BRD4 expression.

journal_name

Int J Chron Obstruct Pulmon Dis

journal_title

International journal of chronic obstructive pulmonary disease

authors

Liu X,Wang J,Luo H,Xu C,Chen X,Zhang R

doi

10.2147/COPD.S278553

subject

Has Abstract

pub_date

2020-12-31 00:00:00

pages

3407-3416

eissn

1176-9106

issn

1178-2005

pii

278553

journal_volume

15

pub_type

杂志文章

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