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Evidence for CD04+ T Cell Methylation Signatures of Network-oriented SOCS3, ITGAL, and NR4A2 Genes with Hemodynamics in Patients with Pulmonary Arterial Hypertension (Array2 DataSet)

ABSTRACT: We hypothesized that methylation dynamics in circulating CD04+ T cells may underlie a precise transcriptional reprogramming that associates with the cardiopulmonary hemodynamic profile of affected patients. We aimed at profiling DNA methylome of circulating CD04+ T cells from patients with PAH and controls by integrating network medicine and hemodynamic parameters.

ORGANISM(S): Homo sapiens

PROVIDER: GSE165357 | GEO | 2022/01/31

REPOSITORIES: GEO

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Evidence for CD04+ T Cell Methylation Signatures of Network-oriented SOCS3, ITGAL, and NR4A2 Genes with Hemodynamics in Patients with Pulmonary Arterial Hypertension (RRBS DataSet)

Project description:We hypothesized that methylation dynamics in circulating CD04+ T cells may underlie a precise transcriptional reprogramming that associates with the cardiopulmonary hemodynamic profile of affected patients. We aimed at profiling DNA methylome of circulating CD04+ T cells from patients with PAH and controls by integrating network medicine and hemodynamic parameters.

2022-01-31 | GSE165358 | GEO

Evidence for CD04+ T Cell Methylation Signatures of Network-oriented SOCS3, ITGAL, and NR4A2 Genes with Hemodynamics in Patients with Pulmonary Arterial Hypertension (Array1 DataSet)

2022-01-31 | GSE165356 | GEO

Evidence for CD04+ T Cell Methylation Signatures of Network-oriented SOCS3, ITGAL, and NR4A2 Genes with Hemodynamics in Patients with Pulmonary Arterial Hypertension

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

2022-01-31 | GSE165360 | GEO

Evidence for CD04+ T Cell Methylation Signatures of Network-oriented SOCS3, ITGAL, and NR4A2 Genes with Hemodynamics in Patients with Pulmonary Arterial Hypertension

Project description:Evidence for CD04+ T Cell Methylation Signatures of Network-oriented SOCS3, ITGAL, and NR4A2 Genes with Hemodynamics in Patients with Pulmonary Arterial Hypertension

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Evidence for CD04+ T Cell Methylation Signatures of Network-oriented SOCS3, ITGAL, and NR4A2 Genes with Hemodynamics in Patients with Pulmonary Arterial Hypertension (RRBS DataSet)

Project description:Evidence for CD04+ T Cell Methylation Signatures of Network-oriented SOCS3, ITGAL, and NR4A2 Genes with Hemodynamics in Patients with Pulmonary Arterial Hypertension (RRBS DataSet)

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Evidence for CD04+ T Cell Methylation Signatures of Network-oriented SOCS3, ITGAL, and NR4A2 Genes with Hemodynamics in Patients with Pulmonary Arterial Hypertension (Array1 DataSet)

| PRJNA694155 | ENA

Evidence for CD04+ T Cell Methylation Signatures of Network-oriented SOCS3, ITGAL, and NR4A2 Genes with Hemodynamics in Patients with Pulmonary Arterial Hypertension (Array2 DataSet)

| PRJNA694158 | ENA

Endothelial matrix-metalloproteinase-10 promotes pulmonary arterial hypertension associated with systemic sclerosis

Project description:Pulmonary endothelial dysfunction plays an integral role in mediating the initiation and progression of pulmonary vascular remodelling, an important feature of pulmonary arterial hypertension (PAH). Our aim was to decipher the gene expression program of endothelial cells derived from circulating endothelial progenitor (EPCs) to gain insight into the pathological process of PAH associated with systemic sclerosis (SSc), which is the most extreme vascular phenotype of this disease. We used microarrays to investigate the gene expression profile in late outgrowth EPC-derived endothelial cells issued from SSc-PAH patients, in comparison with SSc patients without PAH and healthy controls.

2016-09-30 | GSE73674 | GEO

Human Neutrophils in Pulmonary Arterial Hypertension by LC-MSMS

Project description:Neutrophil elastase (NE) is implicated in pulmonary arterial hypertension (PAH) but the role of neutrophils in the pathogenesis of PAH is unclear. Here we show that neutrophils from PAH vs. control subjects produce and release increased NE associated with enhanced extracellular trap formation. PAH neutrophils are highly adherent and show decreased migration consistent with increased vinculin, identified on proteomic analysis and previously linked to an antiviral response. This was substantiated by a transcriptomic interferon signature in PAH neutrophils and an increase in human endogenous retrovirus (HERV-K) envelope protein. NE and interferon genes are induced by HERV-K envelope and vinculin is increased by HERV-K dUTPase that is elevated in PAH plasma. Neutrophil exosomes from PAH plasma contain increased NE and HERV-K envelope and induce pulmonary hypertension in mice, that is mitigated by the NE inhibitor and antiviral agent, elafin. Thus elevated HERVs explain pathological neutrophils linked to PAH induction and progression.

2023-03-11 | PXD023134 | Pride

Transcription profiling by array of human BMPR2 mutation carriers with and without evidence of pulmonary arterial hypertension

Project description:Background: While BMPR2 mutation strongly predisposes to pulmonary arterial hypertension (PAH), only 20% of mutation carriers develop clinical disease. This finding suggests that modifier genes contribute to FPAH clinical expression. Since modifiers are likely to be common alleles, this problem is not tractable by traditional genetic approaches. Further, examination of gene expression is complicated by confounding effects attributable to drugs and the disease process itself. Methods: To resolve these problems, B-cells were isolated, EBV-immortalized, and cultured from familial PAH patients with BMPR2 mutations, mutation positive but disease-free family members, and family members without mutation. This allows examination of differences in gene expression without drug or disease-related effects. These differences were assayed by Affymetrix array, with follow-up by quantitative RT-PCR and additional statistical analyses. Results: By gene array, we found consistent alterations in multiple pathways with known relationship to PAH, including actin organization, immune function, calcium balance, growth, and apoptosis. Selected genes were verified by quantitative RT-PCR using a larger sample set. Analysis of overrepresented gene ontology groups suggests that it is pathway-specific, not gene-specific changes that carry increased risk of disease. Conclusions: B-cell lines are a valuable and accessible tool for assaying alterations in gene expression free from drug and disease effects. Predisposition to disease within BMPR2 mutation carriers was linked to several pathways, including proliferation, GTP signaling, and stress response. Experiment Overall Design: Immortalized B-cells from BMPR2 mutation carriers with and without disease are compared to search for modifier genes

2008-10-25 | E-GEOD-10767 | biostudies-arrayexpress

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