Transcriptomics analysis of lung samples of COPD patients identifies shared pathways involved in the disease among independent studies

سال انتشار: 1402
محل انتشار: دوازدهمین همایش ملی و سومین همایش بین المللی بیوانفورماتیک
کد COI اختصاصی: IBIS12_080
زبان مقاله: انگلیسی
تعداد مشاهده: 113

نویسندگان

Department of Cell and Molecular Biology, Faculty of Life Sciences and Biotechnology, Shahid BeheshtiUniversity, Tehran, Iran

Masoud Arabfard

Chemical Injuries Research Center, Systems Biology and Poisonings Institute, Baqiyatallah University ofMedical Sciences, Tehran, Iran

چکیده

Chronic obstructive pulmonary disease (COPD) manifests as a heterogeneous diseasedistinguished by enduring respiratory symptoms attributable to structural anomalies affecting theairways and alveoli. These anomalies give rise to persistent airflow obstruction, often exhibiting aprogressive nature(۱). Individuals who engage in cigarette smoking, the most prominent risk factor forCOPD, generally experience pulmonary inflammation. However, those who develop COPDdemonstrate a heightened or aberrant response to inhaling toxic agents(۲, ۳). Differentially expressedgenes play a role in various pathogenesis pathways, including those responsible for inflammation(۴). Inthe present study, we employed a transcriptomics merge-analysis approach to identify the DifferentiallyExpressed Genes (DEGs) and their associated pathways. Two microarray datasets, GSE۳۸۹۷۴ andGSE۲۷۵۹۷, published in ۲۰۱۲ and ۲۰۱۱, respectively, were used in the differential expression analysis.The merged data encompassed a total of ۱۷ normal smokers and ۷۱ COPD smoker patients. The resultsof the Differentially Expressed Genes (DEG) analysis using criteria of |logFC| > ۱ and Adjusted p-value< ۰.۰۵ revealed ۳۵ upregulated and ۳۷ downregulated genes between normal smokers and COPDsmoker patients. Furthermore, the differentially expressed genes were involved in several pathwayscontributing to COPD pathogenesis such as TNF, IL-۱۷, Chemokine, C-type lectin receptor, NF-kappaβ, and Toll-like receptor signaling pathways (Adjusted p-value < ۰.۰۰۱).

کلیدواژه ها

COPD; Lung Tissue; Transcriptome Analysis

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