8Įmerging studies showed that the genetic factors are also important determinants of COPD. Recently, microRNA-21 was reported to mediate COPD pathogenesis by regulating SATB1/S100A9/NF-κB axis. 7 Moreover, the study showed that MicroRNA-218 regulated the overproduction of MUC5AC and inflammation of COPD by targeting TNFR1-mediated NF-κB pathway. 6 The distinct miRNA profile was also observed in COPD. The aging-related genes were also differently expressed in COPD. 5 A microarray of epithelium from COPD survey the TLR family gene expression and revealed that TLR5 is essential for the activation of innate immune responses in COPD. The dysregulation of mRNA and miRNA expression was also observed in COPD. The underlying pathophysiological mechanism is urgent for developing new therapies for COPD. 4 However, the pathological mechanism of COPD remains limited. 3 Although smoking and aging are the main causes of COPD. 2 As the COPD is often punctuated by rhinoviruses (RVs), the acute exacerbations frequently lead to morbidity and mortality of these patients. 1 The prevalence of COPD is increasingly worldwide, which become a great individual and society burden. Keywords: chronic obstructive pulmonary disease, lncRNA, miRNA, bioinformaticsĬhronic obstructive pulmonary disease (COPD) is a common chronic bronchitis or emphysema hallmarked by chronic respiratory symptoms and airflow restriction, which can further develop into common chronic diseases of pulmonary heart disease and respiratory failure. And the cytoHubba analysis identified ATM, SMAD7 and HIF1A as hub genes of ceRNA network.Ĭonclusion: This study provides a landscape of ceRNA network of COPD, which help to reveal the underlying pathophysiological mechanisms of COPD and shed light on novel therapeutic strategies for COPD. The hub-lncRNA (the network is ranked in the top 10) as the core marker of COPD, including SNHG12, SLFNL1-AS1, KCNQ1OT1, XIST, EAF1-AS1, FOXD2-AS1, NORAD, PINK1-AS and RP11-69E11.4. Next, a ceRNA network including 93 DEGs, 2 DEmi, 463 lncRNAs, and 1157 DEG-lncRNA, DEmi-lncRNA, and DEmi-DEG interactions were obtained. Hallmark enrichment showed that chronic neutrophil inflammation was a sign of the pathogenesis of COPD. KEGG pathway enrichment shows that the p53 pathway was upregulated in COPD. GO enrichment showed that leukocyte chemotaxis, cell chemotaxis, and myeloid leukocyte migration were upregulated, and muscle and membrane repolarization-related biological progress were downregulated in COPD. Results: Firstly, the 519 DEGs and 17 DEmis were identified from COPD GEO datasets. #DIFFERENCE BETWEEN ABSCISSA AND ORDINATE SOFTWARE#Finally, the Cytoscape software was used to analyze the network topology and COPD-related lncRNAs. Subsequently, the COPD-related ceRNA network was constructed based on the interaction between lncRNA, miRNA, and mRNA using the lncACTdb database. Methods: We obtained the gene expression profile and miRNA expression profile of COPD patients from Gene Expression Omnibus (GEO) database, and the differentially expressed genes (DEGs) and differentially expressed miRNAs (DEmis) in COPD were identified. However, the molecular mechanism of COPD needs to be further revealed. 1 Tongdao North Street, Huimin District, Hohhot, 010010, Inner Mongolia Autonomous Region, People’s Republic of China, Email īackground: Chronic obstructive pulmonary disease (COPD) is a common chronic disease of the respiratory tract, with high prevalence, high disability, and poor prognosis. Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, People’s Republic of ChinaĬorrespondence: Lu Hao, Area B, Department of Respiratory Medicine, Affiliated Hospital of Inner Mongolia Medical University, No.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |