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Epigenome‑wide association study on asthma and chronic obstructive pulmonary disease overlap reveals aberrant DNA methylations related to clinical phenotypes

ABSTRACT: Epigenome‑wide association study on asthma and chronic obstructive pulmonary disease overlap reveals aberrant DNA methylations related to clinical phenotypes

PROVIDER: PRJNA485734 | ENA |

REPOSITORIES: ENA

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Epigenome‑wide association study on asthma and chronic obstructive pulmonary disease overlap reveals aberrant DNA methylations related to clinical phenotypes

Project description:Genome wide DNA methylation profiling of Chronic Obstructive Pulmonary Disease (COPD) patients and healthy subjects. The Illumina Infinium HumanMethylation450 BeadChip was used to obtain DNA methylation profiles across in peripheral blood mononuclear cell samples. Samples included 6 normal subjects and 12 COPD patients among which 3 of them have 2nd samples from follow-up examination.

2021-03-08 | GSE118468 | GEO

Epigenome-wide association study on asthma and chronic obstructive pulmonary disease overlap reveals aberrant DNA methylations related to clinical phenotypes.

Project description:We hypothesized that epigenetics is a link between smoking/allergen exposures and the development of Asthma and chronic obstructive pulmonary disease (ACO). A total of 75 of 228 COPD patients were identified as ACO, which was independently associated with increased exacerbations. Microarray analysis identified 404 differentially methylated loci (DML) in ACO patients, and 6575 DML in those with rapid lung function decline in a discovery cohort. In the validation cohort, ACO patients had hypermethylated PDE9A (+ 30,088)/ZNF323 (- 296), and hypomethylated SEPT8 (- 47) genes as compared with either pure COPD patients or healthy non-smokers. Hypermethylated TIGIT (- 173) gene and hypomethylated CYSLTR1 (+ 348)/CCDC88C (+ 125,722)/ADORA2B (+ 1339) were associated with severe airflow limitation, while hypomethylated IFRD1 (- 515) gene with frequent exacerbation in all the COPD patients. Hypermethylated ZNF323 (- 296) / MPV17L (+ 194) and hypomethylated PTPRN2 (+ 10,000) genes were associated with rapid lung function decline. In vitro cigarette smoke extract and ovalbumin concurrent exposure resulted in specific DNA methylation changes of the MPV17L / ZNF323 genes, while 5-aza-2'-deoxycytidine treatment reversed promoter hypermethylation-mediated MPV17L under-expression accompanied with reduced apoptosis and decreased generation of reactive oxygen species. Aberrant DNA methylations may constitute a determinant for ACO, and provide a biomarker of airflow limitation, exacerbation, and lung function decline.

| S-EPMC7930096 | biostudies-literature

Airway and parenchyma RNA sequencing in a mouse model of asthma chronic obstructive pulmonary disease overlap

Project description:To profile airway and parenchyma transcriptomes in our mouse model of asthma chronic obstructive pulmonary disease overlap, we employed RNA-Seq (TruSeq Stranded mRNA sample preparation, NovaSeq 6000, 20 million 100 bp single reads) as a discovery tool to identify mRNAs of interest in the development of experimental asthma chronic obstructive pulmonary disease overlap. Experimental asthma: Some mice were sensitized and challenged intranasally with house dust mite (HDM) extract 5 days per week for 3 weeks. In other mice, this was HDM treatment 3 times/week from weeks 4-11. Controls received phosphate buffered saline (PBS). Experimental chronic obstructive pulmonary disease (COPD): Mice were exposed to cigarette smoke (CS) twice per day, 5 days per week for 8 weeks. Control mice were exposed to normal air (AIR). Experimental asthma-COPD overlap (ACO): Mice were sensitized and challenged intranasally with HDM or PBS. From weeks 4-11, mice were also exposed to CS or AIR. Treatment with dexamethasone (DEX): Separate groups of mice were treated with DEX during week 11. Lungs were excised, airway and parenchyma tissue were isolated through blunt dissection, and total RNA isolated.

2023-02-01 | GSE199853 | GEO

Proteomic analysis of human eosinophils in patients with asthma-COPD overlap and eosinophilic COPD

Project description:Activated eosinophils is a major cell type to be mainly involved in allergic diseases. Recent studies also indicated that eosinophils play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD), especially asthma-COPD overlap and/or eosinophil COPD. The aim of this study is to clarify cellular characters of human eosinophils in patients with asthma-COPD overlap and/or eosinophil COPD.

2024-06-20 | PXD052550 | JPOST Repository

Airway and parenchyma RNA sequencing in a mouse model of asthma chronic obstructive pulmonary disease overlap

Project description:Airway and parenchyma RNA sequencing in a mouse model of asthma chronic obstructive pulmonary disease overlap

| PRJNA821727 | ENA

Human Obstructive and Non-obstructive Hypertrophic Cardiomyopathy Disease Mechanisms

Project description:To understand the interplay between cardiomyocyte and nonmyocyte cell types in human obstructive and non-obstructive hypertrophic cardiomyopathy, single nuclei RNA-sequencing was performed on 2 unused donor hearts, 1 obstructive HCM specimen, and 6 non-obstructive HCM specimens.

2022-01-01 | GSE181764 | GEO

Asthma, chronic obstructive pulmonary disease, and asthma-COPD overlap among US working adults.

Project description:BackgroundAsthma-COPD overlap (ACO) is a respiratory condition with more severe respiratory symptoms, poorer quality of life, and increased hospital admissions compared with asthma or COPD alone.ObjectivesEstimate asthma, chronic obstructive pulmonary disease (COPD), and ACO prevalence among workers by industry and occupation and assess physical and mental health status, healthcare utilization, among workers with ACO.MethodsThe 2014-2018 National Health Interview Survey (NHIS) data for working adults aged ≥18 years employed (sample n = 99,424) in the 12 months prior to the survey were analyzed. Age-adjusted ACO, COPD and asthma prevalence and prevalence ratios adjusted for age, sex, race and smoking status were estimated.ResultsDuring 2014-2018, of the estimated 166 million (annual average) US workers, age-adjusted asthma, COPD, and ACO prevalence was 6.9%, 4.0%, and 1.1%, respectively. ACO prevalence was highest among workers aged ≥65 years (2.0%), females (1.6%), current smokers (1.9%), those living below the federal poverty level (2.3%), and workers in the accommodation and food services (1.6%) industry and personal care and service (2.3%) occupations. Workers with ACO had more frequent (p < 0.05) physician office visits, emergency department visits; and were more likely to be in poorer mental health, obese, have more lost workdays, more bed days, and comorbidities compared to workers with asthma alone and workers with COPD alone.Conclusion: Higher ACO prevalence among worker groups and increased healthcare utilization underscores the need for early identification of asthma and COPD, assessment of potential workplace exposures, and implementation of tailored interventions to reduce ACO among working adults.

| S-EPMC10664241 | biostudies-literature

Human Obstructive and Non-obstructive Hypertrophic Cardiomyopathy Disease Mechanisms

Project description:Human Obstructive and Non-obstructive Hypertrophic Cardiomyopathy Disease Mechanisms

| PRJNA753316 | ENA

Transcriptome analysis of sputum cells reveals two distinct molecular phenotypes of "asthma and chronic obstructive pulmonary disease overlap" in the elderly.

Project description:BackgroundLittle is known about the pathogenesis of asthma and chronic obstructive pulmonary disease (COPD) overlap (ACO). This study examined the molecular phenotypes of ACO in the elderly.MethodsA genome-wide investigation of gene expression in sputum cells from the elderly with asthma, ACO, or COPD was performed using gene set variation analysis (GSVA) with predefined asthma- or COPD-specific gene signatures. We then performed a subsequent cluster analysis using enrichment scores (ESs) to identify molecular clusters in the elderly with ACO. Finally, a second GSVA was conducted with curated gene signatures to gain insight into the pathogenesis of ACO associated with the identified molecular clusters.ResultsSeventy elderly individuals were enrolled (17 with asthma, 41 with ACO, and 12 with COPD). Two distinct molecular clusters of ACO were identified. Clinically, ACO cluster 1 (N = 23) was characterized by male and smoker dominance, more obstructive lung function, and higher proportions of both neutrophil and eosinophil in induced sputum compared to ACO cluster 2 (N = 18). ACO cluster 1 had molecular features similar to both asthma and COPD, with mitochondria and peroxisome dysfunction as important mechanisms in the pathogenesis of these diseases. The molecular features of ACO cluster 2 differed from those of asthma and COPD, with enhanced innate immune reactions to microorganisms identified as being important in the pathogenesis of this form of ACO.ConclusionRecognition of the unique biological pathways associated with the two distinct molecular phenotypes of ACO will deepen our understanding of ACO in the elderly.

| S-EPMC9617312 | biostudies-literature

Substoichiometric ribose methylations in spliceosomal snRNAs

Project description:Substoichiometric ribose methylations in spliceosomal snRNAs

| PRJNA414213 | ENA