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      Microarray analysis of lung long non-coding RNAs in cigarette smoke-exposed mouse model

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          Abstract

          Several studies have demonstrated the function of long non‑coding RNAs (lncRNAs) in various biological processes, yet their role underlying the susceptibility to cigarette smoke (CS)-induced airway inflammation remains limited. In the present study, we aimed to profile the expression of lncRNAs and mRNAs in CS-exposed mice. C57BL/6 mice were assigned into a single cigarette-smoking machine with or without CS exposure for 4 weeks, followed by lung tissue harvest and RNA isolation. Microarray analysis identified 108 lncRNAs and 119 mRNAs with differential expression levels in CS-exposed mouse lung tissue compared with those in control mice. The expression patterns of several lncRNAs were further confirmed by qRT-PCR. GO and pathway analyses showed that the altered mRNAs were mainly related to the processes of immune response, defense response and cell chemotaxis, cytokine-cytokine receptor interaction and chemokine signaling pathway. Moreover, a single lncRNA may co-expressed with several mRNAs, and so was the mRNA. Our findings uncovered the expression profile of lncRNAs and mRNAs in the lungs of CS-exposed mice, which may offer new insights into pathogenesis of CS-associated airway inflammatory disorders.

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          Most cited references24

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          Immunologic aspects of chronic obstructive pulmonary disease.

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            Alarmins: chemotactic activators of immune responses.

            The recruitment and activation of antigen-presenting cells are critical early steps in mounting an immune response. Many microbial components and endogenous mediators participate in this process. Recent studies have identified a group of structurally diverse multifunctional host proteins that are rapidly released following pathogen challenge and/or cell death and, most importantly, are able to both recruit and activate antigen-presenting cells. These potent immunostimulants, including defensins, cathelicidin, eosinophil-derived neurotoxin, and high-mobility group box protein 1, serve as early warning signals to activate innate and adaptive immune systems. We propose to highlight these proteins' unique activities by grouping them under the novel term 'alarmins', in recognition of their role in mobilizing the immune system.
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              Multifaceted mechanisms in COPD: inflammation, immunity, and tissue repair and destruction.

              Chronic obstructive pulmonary disease is a leading global cause of morbidity and mortality that is characterised by inexorable deterioration of small airways obstruction with emphysema associated with cellular inflammation and structural remodelling. Other features include apoptosis as well as proliferation of cells, and both tissue repair and lack of tissue repair. Metalloprotease release, together with that of apoptotic factors, may underlie the emphysema, and, conversely, fibrosis of the small airways may be accounted for by the effects of growth factor activation. In advanced disease, influential factors include the development of autoimmunity, with activation of dendritic cells and T-helper cells of both type 1 and 2, and the senescence response. An inability of macrophages to ingest apoptosed cells and bacteria may exacerbate inflammatory responses. Systemic inflammation with concomitant cardiovascular disease and metabolic syndrome may reflect the effect of cigarette smoke on nonpulmonary cells. Corticosteroid resistance may be secondary to oxidative stress mechanisms, such as inactivation of histone deacetylases. The mechanisms of chronic obstructive pulmonary disease may be heterogeneous, according to severity, and clinical phenotypes need to be correlated with cellular and pathological processes. Treatments may be targeted to patients with specific mechanisms.
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                Author and article information

                Journal
                Oncotarget
                Oncotarget
                Oncotarget
                ImpactJ
                Oncotarget
                Impact Journals LLC
                1949-2553
                29 December 2017
                18 December 2017
                : 8
                : 70
                : 115647-115656
                Affiliations
                1 Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, and Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, Chengdu 610041, China
                Author notes
                Correspondence to: Yongchun Shen, shen_yongchun@ 123456126.com
                Article
                23362
                10.18632/oncotarget.23362
                5777800
                29383188
                69df8093-41a1-4176-bf7c-606102b8ec5b
                Copyright: © 2017 Wang et al.

                This article is distributed under the terms of the Creative Commons Attribution License (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited.

                History
                : 8 September 2017
                : 5 December 2017
                Categories
                Research Paper

                Oncology & Radiotherapy
                long non-coding rnas,cigarette smoke,airway inflammation,mice,microarray analysis

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