Epigenome-wide profiling uncovers novel pathway networks in human pulmonary arterial hypertension [pul36]
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE194080 | GEO | 2022/06/09
REPOSITORIES: GEO
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Project description:Pulmonary arterial hypertension (PAH) is a progressive pulmonary vascular disease that culminates in right heart failure. Vascular pathology in PH is characterized by pulmonary vasoconstriction and progressive vascular remodeling processes that affects all layers of the vascular wall (intima, media and adventitia). Our objective was to profile and analyze the differential gene expression signatures between the cells isolated from normal and idiopathic PAH patients. We generated vascular cell-specific transcriptome profiles from the adventitial fibroblasts (PAAF) isolated ex vivo from the dissected human pulmonary arteries of normal donor and PAH lungs using paired-end RNA-sequencing.
2022-06-09 | GSE193776 | GEO
Project description:Pulmonary arterial hypertension (PAH) is a progressive pulmonary vascular disease that culminates in right heart failure. Vascular pathology in PH is characterized by pulmonary vasoconstriction and progressive vascular remodeling processes that affects all layers of the vascular wall (intima, media and adventitia). Our objective was to profile and analyze the differential gene expression signatures between the cells isolated from normal and idiopathic PAH patients. We generated vascular cell-specific transcriptome profiles from the adventitial fibroblasts (PAAF) isolated ex vivo from the dissected human pulmonary arteries of normal donor and PAH lungs using paired-end RNA-sequencing.
2022-06-09 | GSE194079 | GEO
Project description:Pulmonary arterial hypertension (PAH) is a progressive pulmonary vascular disease that culminates in right heart failure. Vascular pathology in PH is characterized by pulmonary vasoconstriction and progressive vascular remodeling processes that affects all layers of the vascular wall (intima, media and adventitia). Our objective was to profile and analyze the differential gene expression signatures between the cells isolated from normal and idiopathic PAH patients. We generated vascular cell-specific transcriptome profiles from the adventitial fibroblasts (PAAF) isolated ex vivo from the dissected human pulmonary arteries of normal donor and PAH lungs using paired-end RNA-sequencing.
2022-06-09 | GSE194067 | GEO
Project description:Pulmonary arterial hypertension (PAH) is a progressive pulmonary vascular disease that culminates in right heart failure. Vascular pathology in PH is characterized by pulmonary vasoconstriction and progressive vascular remodeling processes that affects all layers of the vascular wall (intima, media and adventitia). Our objective was to profile and analyze the differential gene expression signatures between the cells isolated from normal and idiopathic PAH patients. We generated vascular cell-specific transcriptome profiles from the adventitial fibroblasts (PAAF) isolated ex vivo from the dissected human pulmonary arteries of normal donor and PAH lungs using paired-end RNA-sequencing.
2022-06-09 | GSE144935 | GEO
Project description:Pulmonary arterial hypertension (PAH) is a progressive pulmonary vascular disease that culminates in right heart failure. Vascular pathology in PH is characterized by pulmonary vasoconstriction and progressive vascular remodeling processes that affects all layers of the vascular wall (intima, media and adventitia). Our objective was to profile and analyze the differential gene expression signatures between the cells isolated from normal and idiopathic PAH patients. We generated vascular cell-specific transcriptome profiles from the adventitial fibroblasts (PAAF) isolated ex vivo from the dissected human pulmonary arteries of normal donor and PAH lungs using paired-end RNA-sequencing.
2022-06-09 | GSE144932 | GEO
Project description:Pulmonary arterial hypertension (PAH) is a severe and incurable pulmonary vascular disease. One of the primary origins of PAH is pulmonary endothelial dysfunction leading to vasoconstriction, aberrant angiogenesis and smooth muscle cell proliferation, endothelial-to-mesenchymal transition, thrombosis and inflammation. Our objective was to study the epigenetic variations in pulmonary endothelial cells (PEC) through a specific pattern of DNA methylation. DNA was extracted from cultured PEC from patients with idiopathic PAH (n=11), heritable PAH (n=10) and controls (n=18). ). DNA methylation was assessed using the Illumina HumanMethylation450 Assay. After normalization, samples and probes were clustered according to their methylation profile. Differential clusters were functionally analysed using bioinformatics tools.
2016-07-15 | E-GEOD-84395 | biostudies-arrayexpress
Project description:Pulmonary arterial hypertension (PAH) is a severe and incurable pulmonary vascular disease. One of the primary origins of PAH is pulmonary endothelial dysfunction leading to vasoconstriction, aberrant angiogenesis and smooth muscle cell proliferation, endothelial-to-mesenchymal transition, thrombosis and inflammation. Our objective was to study the epigenetic variations in pulmonary endothelial cells (PEC) through a specific pattern of DNA methylation.
2016-07-15 | GSE84395 | GEO
Project description:Idiopathic Pulmonary Arterial Hypertension (IPAH) is a severe human disease, characterized by extensive pulmonary vascular remodeling due to plexiform and obliterative lesions, media hypertrophy, and alterations of adventitia. The objective of the study was to test the hypothesis that microscopic IPAH vascular lesions express unique molecular profiles, which collectively are different from control pulmonary arteries. We used digital spatial transcriptomics to profile the genome-wide differential transcriptomic signature of key pathological lesions (plexiform, obliterative, intima+media hypertrophy, and adventitia) in IPAH lungs (n= 11) and compared these data to the intima+media and adventitia of control pulmonary artery (n=5). The IPAH lesions and pulmonary artery compartments were defined by the analyses of hematoxylin-eosin stained serial section, aided by labeling with CD31 (for endothelial cells), smooth muscle cell actin (SMA), and CD45 for inflammatory mononuclear cells, also in serial sections. Approximately 12 regions of interest (ROI) were sampled from a histological section of a paraffin-embedded block of each lung, which was selected based on the finding of enrichment for IPAH lesions or control pulmonary arteries.
2024-04-04 | GSE256539 | GEO
Project description:Although multiple gene and protein expression have been extensively profiled in human pulmonary arterial hypertension (PAH), the mechanism for the development and progression of pulmonary hypertension remains elusive. Analysis of the global metabolomic heterogeneity within the pulmonary vascular system leads to a better understanding of disease progression. Using a combination of high-throughput liquid-and-gas-chromatography-based mass spectrometry, we showed unbiased metabolomic profiles of disrupted glycolysis, increased TCA cycle, and fatty acid metabolites with altered oxidation pathways in the severe human PAH lung. The results suggest that PAH has specific metabolic pathways contributing to increased ATP synthesis for the vascular remodeling process in severe pulmonary hypertension. These identified metabolites may serve as potential biomarkers for the diagnosis of severe PAH. By profiling metabolomic alterations of the PAH lung, we reveal new pathogenic mechanisms of PAH in its later stage, which may differ from the earlier stage of PAH, opening an avenue of exploration for therapeutics that target metabolic pathway alterations in the progression of PAH. Global profiles were determined in human lung tissue and compared across 11 normal and 12 severe pulmonary arterial hypertension patients. Using a combination of microarray and high-throughput liquid-and-gas-chromatography-based mass spectrometry, we showed unbiased metabolomic profiles of disrupted glycolysis, increased TCA cycle, and fatty acid metabolites with altered oxidation pathways in the severe human PAH lung.
2014-11-14 | E-GEOD-53408 | biostudies-arrayexpress
Project description:Although multiple gene and protein expression have been extensively profiled in human pulmonary arterial hypertension (PAH), the mechanism for the development and progression of pulmonary hypertension remains elusive. Analysis of the global metabolomic heterogeneity within the pulmonary vascular system leads to a better understanding of disease progression. Using a combination of high-throughput liquid-and-gas-chromatography-based mass spectrometry, we showed unbiased metabolomic profiles of disrupted glycolysis, increased TCA cycle, and fatty acid metabolites with altered oxidation pathways in the severe human PAH lung. The results suggest that PAH has specific metabolic pathways contributing to increased ATP synthesis for the vascular remodeling process in severe pulmonary hypertension. These identified metabolites may serve as potential biomarkers for the diagnosis of severe PAH. By profiling metabolomic alterations of the PAH lung, we reveal new pathogenic mechanisms of PAH in its later stage, which may differ from the earlier stage of PAH, opening an avenue of exploration for therapeutics that target metabolic pathway alterations in the progression of PAH.
2014-11-14 | GSE53408 | GEO