DNA methylation profiling in peripheral lung tissues of smokers and patients with COPD

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dc.contributor.author Sundar, Isaac K.
dc.contributor.author Yin, Qiangzong
dc.contributor.author Baier, Brian S.
dc.contributor.author Yan, Li
dc.contributor.author Mazur, Witold
dc.contributor.author Li, Dongmei
dc.contributor.author Susiarjo, Martha
dc.contributor.author Rahman, Irfan
dc.date.accessioned 2017-07-05T11:22:00Z
dc.date.available 2017-07-05T11:22:00Z
dc.date.issued 2017-04-14
dc.identifier.citation Sundar , I K , Yin , Q , Baier , B S , Yan , L , Mazur , W , Li , D , Susiarjo , M & Rahman , I 2017 , ' DNA methylation profiling in peripheral lung tissues of smokers and patients with COPD ' , Clinical epigenetics , vol. 9 , 38 . https://doi.org/10.1186/s13148-017-0335-5
dc.identifier.other PURE: 86548386
dc.identifier.other PURE UUID: 8a03f59c-2c21-42cc-ae41-8be875a1cea1
dc.identifier.other WOS: 000400789000001
dc.identifier.other Scopus: 85018514998
dc.identifier.uri http://hdl.handle.net/10138/197458
dc.description.abstract Background: Epigenetics changes have been shown to be affected by cigarette smoking. Cigarette smoke (CS)-mediated DNA methylation can potentially affect several cellular and pathophysiological processes, acute exacerbations, and comorbidity in the lungs of patients with chronic obstructive pulmonary disease (COPD). We sought to determine whether genome-wide lung DNA methylation profiles of smokers and patients with COPD were significantly different from non-smokers. We isolated DNA from parenchymal lung tissues of patients including eight lifelong non-smokers, eight current smokers, and eight patients with COPD and analyzed the samples using Illumina's Infinium HumanMethylation450 BeadChip. Results: Our data revealed that the differentially methylated genes were related to top canonical pathways (e.g., G beta gamma signaling, mechanisms of cancer, and nNOS signaling in neurons), disease and disorders (organismal injury and abnormalities, cancer, and respiratory disease), and molecular and cellular functions (cell death and survival, cellular assembly and organization, cellular function and maintenance) in patients with COPD. The genome-wide DNA methylation analysis identified suggestive genes, such as NOS1AP, TNFAIP2, BID, GABRB1, ATXN7, and THOC7 with DNA methylation changes in COPD lung tissues that were further validated by pyrosequencing. Pyrosequencing validation confirmed hyper-methylation in smokers and patients with COPD as compared to non-smokers. However, we did not detect significant differences in DNA methylation for TNFAIP2, ATXN7, and THOC7 genes in smokers and COPD groups despite the changes observed in the genome-wide analysis. Conclusions: Our study suggests that DNA methylation in suggestive genes, such as NOS1AP, BID, and GABRB1 may be used as epigenetic signatures in smokers and patients with COPD if the same is validated in a larger cohort. Future studies are required to correlate DNA methylation status with transcriptomics of selective genes identified in this study and elucidate their role and involvement in the progression of COPD and its exacerbations. en
dc.format.extent 18
dc.language.iso eng
dc.relation.ispartof Clinical epigenetics
dc.rights cc_by
dc.rights.uri info:eu-repo/semantics/openAccess
dc.subject DNA methylation
dc.subject Lung
dc.subject Epigenetics
dc.subject COPD
dc.subject Smokers
dc.subject Pyrosequencing
dc.subject CANCER
dc.subject EXPRESSION
dc.subject GENOME
dc.subject 3121 General medicine, internal medicine and other clinical medicine
dc.title DNA methylation profiling in peripheral lung tissues of smokers and patients with COPD en
dc.type Article
dc.contributor.organization Clinicum
dc.contributor.organization University of Helsinki
dc.contributor.organization Department of Medicine
dc.contributor.organization Keuhkosairauksien yksikkö
dc.contributor.organization HUS Heart and Lung Center
dc.description.reviewstatus Peer reviewed
dc.relation.doi https://doi.org/10.1186/s13148-017-0335-5
dc.relation.issn 1868-7083
dc.rights.accesslevel openAccess
dc.type.version publishedVersion

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