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

PURPOSE: 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.