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Airway Aging and Methylation Disruptions in HIV-associated Chronic Obstructive Pulmonary Disease [methylation]

ABSTRACT: Airway Aging and Methylation Disruptions in HIV-associated Chronic Obstructive Pulmonary Disease [methylation]

PROVIDER: PRJNA741119 | ENA |

REPOSITORIES: ENA

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Airway Aging and Methylation Disruptions in HIV-associated Chronic Obstructive Pulmonary Disease

Project description:Airway Aging and Methylation Disruptions in HIV-associated Chronic Obstructive Pulmonary Disease

| PRJNA741116 | ENA

Airway Aging and Methylation Disruptions in HIV-associated Chronic Obstructive Pulmonary Disease [RNA-seq]

Project description:Airway Aging and Methylation Disruptions in HIV-associated Chronic Obstructive Pulmonary Disease [RNA-seq]

| PRJNA741118 | ENA

Airway Aging and Methylation Disruptions in HIV-associated Chronic Obstructive Pulmonary Disease [methylation]

Project description:Purpose:To identify whether accelerated aging can be observed in the airways of PLWH with COPD, manifest by a unique DNA methylation signature. Methods: Bronchial epithelial brushings from PLWH with and without COPD and HIV-uninfected adults with and without COPD (n=76) were profiled for DNA methylation and gene expression. We evaluated global Alu and LINE-1 methylation and calculated the epigenetic age using the Horvath clock and the methylation telomere length estimator. To identify genome-wide differential DNA methylation and gene expression associated with HIV and COPD, robust linear models were used followed by an expression quantitative trait methylation (eQTM) analysis. Results:Epigenetic age acceleration and shorter methylation estimates of telomere length were found in PLWH with COPD compared to PLWH without COPD and uninfected patients with and without COPD. We identified CpG sites, genes, and eQTM-gene pairs associated with the interaction between HIV and COPD. Conclusions: Methylation age acceleration is observed in the airway epithelium of PLWH with COPD, a process that may be responsible for the heightened risk of COPD in this population. Their distinct methylation profile, differing from that observed in patients with COPD alone, suggests a unique pathogenesis to HIV-associated COPD that warrants investigation into the candidate genes identified.

2022-03-18 | GSE178808 | GEO

Airway Aging and Methylation Disruptions in HIV-associated Chronic Obstructive Pulmonary Disease [RNA-seq]

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Airway Aging and Methylation Disruptions in HIV-associated Chronic Obstructive Pulmonary Disease

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-03-18 | GSE178809 | GEO

Chronic obstructive pulmonary disease

Project description:Diaphragm muscles in Chronic Obstructive Pulmonary Disease (COPD) patients undergo an adaptive fast to slow transformation that includes cellular adaptations. This project studies the signaling mechanisms responsible for this transformation. Keywords: other

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Canonical WNT pathway is activated in the airway epithelium in chronic obstructive pulmonary disease

Project description:We report that the canonical WNT pathway is upregulated in the proximal epithelium of patients with chronic obstructive pulmonary disease. Our data were obtained by using redifferentiated airway epithelium in air/liquid interface, and sequencing the transcriptional activity of components of the WNT signalling pathway

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Chronic obstructive pulmonary disease (COPD)

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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.

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Human Obstructive and Non-obstructive Hypertrophic Cardiomyopathy Disease Mechanisms

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