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Epigenome-wide profiling uncovers novel pathway networks in human pulmonary arterial hypertension [pul31]

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE194067 | GEO | 2022/06/09

REPOSITORIES: GEO

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Epigenome-wide profiling uncovers novel pathway networks in human pulmonary arterial hypertension [pul28]

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.

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Epigenome-wide profiling uncovers novel pathway networks in human pulmonary arterial hypertension [pul35]

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Epigenome-wide profiling uncovers novel pathway networks in human pulmonary arterial hypertension [ChIP-seq]

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Epigenome-wide profiling uncovers novel pathway networks in human pulmonary arterial hypertension [RNA-seq]

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Endothelial DNA methalytion signature in pulmonary arterial hypertension

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

Endothelial DNA methalytion signature in pulmonary arterial hypertension

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Digital Spatial Profiling identifies distinct molecular signatures of vascular lesions in Pulmonary Arterial Hypertension

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.

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Project description:Purpose:Pulmonary arterial hypertension secondary to congenital heart disease (CHD-PAH) with systemic-to-pulmonary shunt is characterized by proliferative vascular remodeling. Capillary morphogenesis gene-2 (CMG2) exhibits roles in cell proliferation and apoptosis. The purpose of this study was to determine the possible roles of CMG2 in the pathogenesis of systemic-to-pulmonary shunt induced PAH. Methods Lung tissue sections from CHD-PAH patients, systemic-to-pulmonary shunt induced PAH rat model, CMG2-/- rats, and PASMCs were used. Immunohistochemistry, real time polymerase chain reaction, Western blot, proliferation, apoptosis, and next generation sequencing (NGS) were performed in this study. Results CMG2 expression was reduced in lung tissues and pulmonary arterioles from Eisenmenger’s syndrome patient and rats with systemic-to-pulmonary shunt induced PAH. CMG2-/- rats exhibited heavier PAH and pulmonary vascular remodeling following exposure to systemic-to-pulmonary shunt for 8 weeks. Over-expression of CMG2 in cultured human PASMCs inhibited cell proliferation and promoted apoptosis, while knockdown of CMG2 promoted cell proliferation and inhibited apoptosis. A total of 1319 genes were found to be dysregulated in CMG2-/- rat lungs as detected by NGS. Biological processes influenced by these differentially expressed genes include regulation of blood vessel diameter, vasoconstriction, regulation of blood vessel size, vascular process in circulatory system, etc., and the most prominent pathway regulated is PI3K-Akt signaling pathway. Conclusion Our work identifies a novel role for CMG2 in systemic-to-pulmonary shunt induced PAH based on the findings that CMG2 deficiency could exacerbate systemic-to- pulmonary shunt induced vascular remodeling in the development of PAH. CMG2 may be a potential target for CHD-PAH treatment.

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Identification of Transcriptional markers in Peripheral Blood of Idiopathic PAH Patients

Project description:Pulmonary Arterial Hypertension (PAH) is characterized by progressive increase in pulmonary vascular resistance, right ventricular failure and premature death. Owing to severe complications, lung biopsies cannot be envisioned to characterize the disease. Based on the prominent role of inflammation in PAH development, we used Peripheral Blood Mononuclear Cells (PBMCs) as cell source, and relied on the SOLiD platform of Serial Analysis of Gene Expression (SAGE) for transcriptional profiling

2020-01-18 | E-MTAB-3276 | biostudies-arrayexpress

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