Dynamic gene expressions of peripheral blood mononuclear cells in patients with acute exacerbation of chronic obstructive pulmonary disease: a preliminary study

Wu, Xiaodan; Sun, Xiaoru; Chen, Chengshui; Bai, Chunxue; Wang, Xiangdong

doi:10.1186/s13054-014-0508-y

Cited by 30 publications

(24 citation statements)

References 36 publications

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“…Folate Receptor Gamma ( FOLR3 ) was found to be 15- to 20-fold upregulated during stable COPD and acute exacerbations of COPD in previous studies, [24] although the mechanistic and functional implications of this upregulation are unclear. Differential methylation of Phospholemman ( FXYD1 ) was shown to be associated with COPD in the ICGN cohort by Qiu et al, [15] and this gene was also previously found to be differentially methylated in response to systemic steroid use in COPD [22].…”

Section: Discussionmentioning

confidence: 99%

Differential DNA methylation marks and gene comethylation of COPD in African-Americans with COPD exacerbations

et al. 2016

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BackgroundChronic obstructive pulmonary disease (COPD) is the third-leading cause of death worldwide. Identifying COPD-associated DNA methylation marks in African-Americans may contribute to our understanding of racial disparities in COPD susceptibility. We determined differentially methylated genes and co-methylation network modules associated with COPD in African-Americans recruited during exacerbations of COPD and smoking controls from the Pennsylvania Study of Chronic Obstructive Pulmonary Exacerbations (PA-SCOPE) cohort.MethodsWe assessed DNA methylation from whole blood samples in 362 African-American smokers in the PA-SCOPE cohort using the Illumina Infinium HumanMethylation27 BeadChip Array. Final analysis included 19302 CpG probes annotated to the nearest gene transcript after quality control. We tested methylation associations with COPD case-control status using mixed linear models. Weighted gene comethylation networks were constructed using weighted gene coexpression network analysis (WGCNA) and network modules were analyzed for association with COPD.ResultsThere were five differentially methylated CpG probes significantly associated with COPD among African-Americans at an FDR less than 5 %, and seven additional probes that approached significance at an FDR less than 10 %. The top ranked gene association was MAML1, which has been shown to affect NOTCH-dependent angiogenesis in murine lung. Network modeling yielded the “yellow” and “blue” comethylation modules which were significantly associated with COPD (p-value 4 × 10-10 and 4 × 10-9, respectively). The yellow module was enriched for gene sets related to inflammatory pathways known to be relevant to COPD. The blue module contained the top ranked genes in the concurrent differential methylation analysis (FXYD1/LGI4, gene significance p-value 1.2 × 10-26; MAML1, p-value 2.0 × 10-26; CD72, p-value 2.1 × 10-25; and LPO, p-value 7.2 × 10-25), and was significantly associated with lung development processes in Gene Ontology gene-set enrichment analysis.ConclusionWe identified 12 differentially methylated CpG sites associated with COPD that mapped to biologically plausible genes. Network module comethylation patterns have identified candidate genes that may be contributing to racial differences in COPD susceptibility and severity. COPD-associated comethylation modules contained genes previously associated with lung disease and inflammation and recapitulated known COPD-associated genes. The genes implicated by differential methylation and WGCNA analysis may provide mechanistic targets contributing to COPD susceptibility, exacerbations, and outcomes among African-Americans.Trial registrationTrial Registration: NCT00774176, Registry: ClinicalTrials.gov, URL: www.clinicaltrials.gov, Date of Enrollment of First Participant: June 2004, Date Registered: 04 January 2008 (retrospectively registered).Electronic supplementary materialThe online version of this article (doi:10.1186/s12931-016-0459-8) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Differential DNA methylation marks and gene comethylation of COPD in African-Americans with COPD exacerbations

et al. 2016

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“…18 In order to face the major challenge that most clinical information was descriptive and unmatched with the digital quantity of omics data, clinical phenomes were scored by DESS and integrated with genomic and proteomic data of patients with acute respiratory distress syndrome and chronic obstructive pulmonary disease. [19][20][21][22] Clinical phenomes were furthermore integrated with lipidomic profiles in patients with pulmonary embolism, acute pneumonia, and acute exacerbation of chronic obstructive pulmonary diseases, based on clinical trans-omics principle. 15 Lipidomic profiles difference between health and lung cancer has been defined and it depends upon methodologies of measurement and analysis, sample preparations and sources, and patient populations and status.…”

Section: Discussionmentioning

confidence: 99%

Trans‐omic profiling between clinical phenoms and lipidomes among patients with different subtypes of lung cancer

Zhu

Zhang

et al. 2020

Clinical & Translational Med

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Lung cancer has high mortality, often accompanied with systemic metabolic disorders. The present study aimed at defining values of trans‐nodules cross‐clinical phenomic and lipidomic network layers in patients with adenocarcinoma (ADC), squamous cell carcinomas, or small cell lung cancer (SCLC). We measured plasma lipidomic profiles of lung cancer patients and found that altered lipid panels and concentrations varied among lung cancer subtypes, genders, ages, stages, metastatic status, nutritional status, and clinical phenome severity. It was shown that phosphatidylethanolamine elements (36:2, 18:0/18:2, and 18:1/18:1) were SCLC specific, whereas lysophosphatidylcholine (20:1 and 22:0 sn‐position‐1) and phosphatidylcholine (19:0/19:0 and 19:0/21:2) were ADC specific. There were statistically more lipids declined in male, <60 ages, late stage, metastasis, or body mass index < 22 . Clinical trans‐omics analyses demonstrated that one phenome in lung cancer subtypes might be generated from multiple metabolic pathways and metabolites, whereas a metabolic pathway and metabolite could contribute to different phenomes among subtypes, although those needed to be furthermore confirmed by bigger studies including larger population of patients in multicenters. Thus, our data suggested that trans‐omic profiles between clinical phenomes and lipidomes might have the value to uncover the heterogeneity of lipid metabolism among lung cancer subtypes and to screen out phenome‐based lipid panels as subtype‐specific biomarkers.

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“…We identified AECOPD-specific biomarkers by evaluating the dynamic gene profiling of peripheral blood mononuclear cells from patients with AECOPD on day 1, 3, and 10 after the hospital admission, as compared with healthy controls or patients with stable COPD [65]. We found that 14 genes were co-differentially up-expressed and 2 downexpressed over tenfold in patients with COPD or AECOPD, as compared with the healthy.…”

Section: Roles Of Ceacam1 In Copdmentioning

confidence: 95%

“…catarrhalis could induce apoptosis in human epithelial cells, which is triggered by interaction between CEACAM1 and ubiquitous surface protein A1 of M. catarrhalis [65]. M. catarrhalis-induced apoptosis as one of pathogenesis of COPD is enhanced by CEACAM1 and mitochondrial death pathways [66,67].…”

Section: Roles Of Ceacam1 In Copdmentioning

confidence: 99%

Roles of CEACAM1 in cell communication and signaling of lung cancer and other diseases

Wang

et al. 2015

Cancer Metastasis Rev

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Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is a broadly-expressed immunoglobulin-like cell adhesion molecule with a wide range of biological functions to regulate cell signaling. The present article mainly focuses on the role of CEACAM1 as a therapeutic target in lung diseases and discusses the potential of therapeutic strategies targeting CEACAM1. The article overviews the structure and its sub-types, biological function, and potential roles of CEACAM1 in lung diseases. Alterations of CEACAM1 expression and CEACAM1-S/CEACAM1-L ratio promote the growth and metastasis of non-small cell lung carcinoma (NSCLC). Moreover, CEACAM1 mediates bacterial adherence and transcellular transcytosis, resulting in the suppression of immune cell activities and inflammatory responses, which may trigger acute exacerbation of chronic obstructive pulmonary disease (AECOPD). CEACAM1 plays a critical role in the development of NSCLC and AECOPD and can be a diagnostic biomarker and therapeutic target in lung diseases.

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Dynamic gene expressions of peripheral blood mononuclear cells in patients with acute exacerbation of chronic obstructive pulmonary disease: a preliminary study

Cited by 30 publications

References 36 publications

Differential DNA methylation marks and gene comethylation of COPD in African-Americans with COPD exacerbations

Differential DNA methylation marks and gene comethylation of COPD in African-Americans with COPD exacerbations

Trans‐omic profiling between clinical phenoms and lipidomes among patients with different subtypes of lung cancer

Roles of CEACAM1 in cell communication and signaling of lung cancer and other diseases

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