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      Is Open Access

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

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          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.

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          Most cited references 29

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          MicroRNAs: target recognition and regulatory functions.

           David Bartel (2009)
          MicroRNAs (miRNAs) are endogenous approximately 23 nt RNAs that play important gene-regulatory roles in animals and plants by pairing to the mRNAs of protein-coding genes to direct their posttranscriptional repression. This review outlines the current understanding of miRNA target recognition in animals and discusses the widespread impact of miRNAs on both the expression and evolution of protein-coding genes.
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            New insights into the immunology of chronic obstructive pulmonary disease.

            Chronic obstructive pulmonary disease (COPD) is a heterogeneous syndrome associated with abnormal inflammatory immune responses of the lung to noxious particles and gases. Cigarette smoke activates innate immune cells such as epithelial cells and macrophages by triggering pattern recognition receptors, either directly or indirectly via the release of damage-associated molecular patterns from stressed or dying cells. Activated dendritic cells induce adaptive immune responses encompassing T helper (Th1 and Th17) CD4+ T cells, CD8+ cytotoxicity, and B-cell responses, which lead to the development of lymphoid follicles on chronic inflammation. Viral and bacterial infections not only cause acute exacerbations of COPD, but also amplify and perpetuate chronic inflammation in stable COPD via pathogen-associated molecular patterns. We discuss the role of autoimmunity (autoantibodies), remodelling, extracellular matrix-derived fragments, impaired innate lung defences, oxidative stress, hypoxia, and dysregulation of microRNAs in the persistence of the pulmonary inflammation despite smoking cessation. Copyright © 2011 Elsevier Ltd. All rights reserved.
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              • Record: found
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              • Article: not found

              Immunologic aspects of chronic obstructive pulmonary disease.

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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                copd
                copd
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove
                1176-9106
                1178-2005
                31 December 2020
                2020
                : 15
                : 3407-3416
                Affiliations
                [1 ]Department of Respiratory, The Second People’s Hospital of Lanzhou City , Lanzhou City, Gansu Province, People’s Republic of China
                [2 ]Department of Interventional Medicine and Oncology, The Affiliated Hospital of Northwest Minzu University , Lanzhou City, Gansu Province, People’s Republic of China
                [3 ]Department of Interventional Medicine and Oncology, Gansu Second People’s Hospital , Lanzhou City, Gansu Province, People’s Republic of China
                Author notes
                Correspondence: Rongxuan Zhang Department of Respiratory, The Second People’s Hospital of Lanzhou City , No. 388 Jiangyuan Road, Chengguan District, Gansu Province730030, People’s Republic of ChinaTel +86-18194260886 Email rvz4rki@163.com
                Article
                278553
                10.2147/COPD.S278553
                7781039
                © 2020 Liu et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 6, Tables: 1, References: 29, Pages: 10
                Funding
                Funded by: No funding;
                No funding was received.
                Categories
                Original Research

                Respiratory medicine

                cigarette smoke extract, mir-218, copd, brd4

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