PTPLAD2 and USP49 Involved in the Pathogenesis of Smoke-Induced COPD by Integrative Bioinformatics Analysis

International Journal of COPD

关键词: copd;    geo;    wgcna;    cigarette;   

DOI  :  

来源: DOAJ

【 摘 要 】

Qiang Zhang,1 Wei Song,1 Nahemuguli Ayidaerhan,2 Zheng He3 1Department of Pulmonary and Critical Care Medicine, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province 110042, People’s Republic of China; 2Department of Pulmonary and Critical Care Medicine, Tarbagatay Prefecture People’s Hospital, Tacheng, Xinjiang, People’s Republic of China; 3Department of Obstetrics and Gynecology Medicine, Shengjing Hospital of China Medical University, Shenyang, People’s Republic of ChinaCorrespondence: Zheng HeDepartment of Obstetrics and Gynecology Medicine, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province 110042, People’s Republic of ChinaEmail [e-mail]: Chronic obstructive pulmonary disease (COPD) is a typical chronic disease, but its molecular pathogenesis remains unclear. This study aimed to investigate the expression of biomarkers during COPD development.Methods: Markers significantly associated with COPD were screened using bioinformatics tools. qRT-PCR and Western blot were used to explore the expression of PTPLAD2 and USP49 in BEAS-2B cells. CCK-8 assay was used to determine the influence of PTPLAD2 and USP49 in BEAS-2B on cell proliferation.Results: In this study, 86 DEGs were identified in GSE76925. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses suggested that the phosphoinositide 3-kinase-Akt signaling pathway, ECM–receptor interaction, mRNA process, and viral transcription were all involved in the development of COPD. In addition, 14 hub genes were identified by WGCNA. PTPLAD2 and USP49 shared DEGs and hub genes and their expression levels were significantly reduced after CSE-treatment in BEAS-2B cells.Conclusion: Our results suggest that PTPLAD2 and USP49 may be useful biomarkers of COPD.Keywords: COPD, GEO, WGCNA, cigarette

【 授权许可】

Unknown