Revealing the target of PASMC from PAH patients and mechanism
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PROVIDER: PRJNA714539 | ENA |
REPOSITORIES: ENA
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Project description:The goal of this study is to identify the target of PAH in PASMC from donor control and PAH patients by transcriptome profiling (RNA-seq) and the mechanism from transcriptome profiling (RNA-seq) and histone modification (ChIPseq)
2021-07-28 | GSE168905 | GEO
Project description:Limited systemic sclerosis patients with pulmonary arterial hypertension show biomarkers of inflammation and vascular injury Forty-nine PBMC samples were obtained from 21 lSSc subjects without PAH (lSSc-noPAH), 15 lSSc subjects with PAH (lSSc-PAH), and 10 healthy controls; three subjects provided PBMCs one year later. Genome-wide gene expression was measured for each sample. Gene expression clearly distinguished lSSc samples from healthy controls, and separated lSSc-PAH from lSSc-NoPAH patients. The gene expression and cytokine profiles of lSSc-PAH patients suggest the presence of activated monocytes, and show markers of vascular injury and inflammation. Sample vs reference, total RNA isolated from peripheral blood mononuclear cells (PBMC), 21 lSSc subjects without PAH (lSSc-noPAH), 15 lSSc subjects with PAH (lSSc-PAH), and 10 healthy controls
2010-10-27 | E-GEOD-19617 | biostudies-arrayexpress
Project description:Limited systemic sclerosis patients with pulmonary arterial hypertension show biomarkers of inflammation and vascular injury Forty-nine PBMC samples were obtained from 21 lSSc subjects without PAH (lSSc-noPAH), 15 lSSc subjects with PAH (lSSc-PAH), and 10 healthy controls; three subjects provided PBMCs one year later. Genome-wide gene expression was measured for each sample. Gene expression clearly distinguished lSSc samples from healthy controls, and separated lSSc-PAH from lSSc-NoPAH patients. The gene expression and cytokine profiles of lSSc-PAH patients suggest the presence of activated monocytes, and show markers of vascular injury and inflammation.
2010-10-27 | GSE19617 | GEO
Project description:To identify dysregulated miRNAs in PAH HPASMC, we compared the miRNA expression profiles between normal and PAH HPASMC using the RT2 miRNA PCR Array System. Total RNA was isolated using a miRNeasy Mini Kit (Qiagen, Valencia, CA) and treated with an RNase-Free DNase Set (Qiagen). After quantification with Nanodrop 2000 spectrophotometer (ThermoScientific, Rockford, IL), miRNAs were reversely transcribed using a RT2 miRNA First Strand Kit (SABiosciences, Frederick, MD). The RT2 miRNA PCR Array System (SABiosciences) was used to study miRNA profiling in normal and PAH HPASMC. U6, SNORD44, SNORD47 and SNORD48 were used as internal controls for the profiling. HPASMC isolated from oe normal donor (C128, as control), one IPAH patient (B157), one PAH patient with Eisenmenger’s syndrome (CC-008) and one PAH patient with Scleroderma (CCF-004) were used for miRNA PCR array study. Data is normalized to the control sample. Three independent sample preparations were used for this study.
2014-02-28 | E-GEOD-55427 | biostudies-arrayexpress
Project description:To identify dysregulated miRNAs in PAH HPASMC, we compared the miRNA expression profiles between normal and PAH HPASMC using the RT2 miRNA PCR Array System.
2014-02-28 | GSE55427 | GEO
Project description:Pregnancy-associated hypertensive (PAH) mice were maintained by mating females carrying the human angiotensinogen (hAGT) gene with males expressing the human renin (hRN) gene, as previously described (Takimoto E., et al., Science, 1996). Angiotensin II (AngII) has critical roles in regulation of blood pressure. In late pregnancy of PAH mice, increased AngII causes acute and severe hypertension with proteinuria. Furthermore, PAH mice show cardiac hypertrophy, fibrosis and apoptosis. It is known that AngII downregulates mRNA of alpha 1a-adrenergic receptor (Adra1a) in neonatal rat cardiac myocytes (Li H.T., et al., Circ. Res., 1997). Interestingly, we found that Adra1a knock out PAH (PAH/aKO) mice display more severe phenotype of cardiac hypertrophy in comparison to PAH mice. In this study, to understand the molecular basis of cardiac hypertrophy via regulation of Adra1a expression with AngII in PAH mice, we performed a comprehensive analysis of gene expression changes in cardiac remodeling of PAH and PAH/aKO mice using the next-generation RNA sequencing (RNA-seq).
2023-01-27 | GSE140948 | GEO
Project description:We report the application of single cell RNA sequencing on human Peripheral Blood Mononuclear cells. The 12 samples are sequenced as biological replications (6 control and 6 patients), and pooled at the analysis stage. The library was prepared using the Chromium Single Cell 3' v2 and v3 Reagent Kit, and sample processing was under bcl2fastq2/2.20.0 and cellranger/2.2.0. We report a decreased CD14 in classical monocytes among PAH patients, with greater potential of apoptosis for CD14+ monocytes population. This study provide a reference for studying the monocytes related abonormalties in PAH and other inflammatory diseases.
2023-06-01 | GSE233189 | GEO
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
Project description:PAH was induced by 60mg/kg MCT and an aorto-caval shunt. At different timepoints of PAH progression (day 14, 21 and 28 after MCT-injection), the left lung with PAH was hemodynamically unloading by unilateral orthotopic transplatation into a syngeneic, healthy recipient. All day 14 and 7/10 day 21 transplanted lungs showed reversal of PAH after LTx. All day 28 and 3/10 day 21 transplanted lungs showed PAH progression after LTx. Lung tissue of Reversible and Irreversible PAH and normal controls, acquired at LTx, was compared using RNA-seq.
2020-07-01 | GSE149899 | GEO
Project description:Background:Pulmonary arterial hypertension (PAH) is a severe condition characterized by progressive vascular remodeling of small pulmonary arteries (PAs) causing sustained elevation of PA pressure, right ventricular failure and death. Similar to cancer cells, PA smooth muscle cells (PASMCs), which play a key role in pulmonary vascular remodeling, have adopted multiple mechanisms to sustain their survival and proliferation in the presence of stress. The histone methyltransferase G9a has been shown to exert oncogenic effects and to serve as a buffer against an exaggerated transcriptional response. Therefore, we hypothesized that G9a up-regulation in PAH plays a pivotal role in pulmonary vascular remodeling by maintaining the abnormal phenotype of PAH-PASMCs. Methods: G9alevels were measured in PAs and isolated PASMCs of PAH patients and animal models. Selective G9a pharmacological inhibitors were used in human PAH-PASMCs and in rodent PAH models (i.e.Fawn-Hooded rats and Sugen/Hypoxia-exposed mice). Results: We present evidence of increased expression of G9a in PASMCs from PAH patients as well as in remodeled PAs from animal models. We found that pharmacological inhibition of G9a activity using BIX01294 and UNC0642significantly reduces the prosurvival and proproliferative potentials of cultured PAH-PASMCs. Using RNA sequencing, further exploration revealed that G9a promotes extracellular matrix production and affords protection against the negative effects of an overactive stress response. Finally, we found that therapeutic treatment with BIX01294 reduced pulmonary vascular remodeling and lowered mean PA pressure in Fawn-Hooded rats. Treatment of Sugen/hypoxia-challenged mice with BIX01294 also improved pulmonary hemodynamics and right ventricular function. Conclusions:These findings suggest that G9a inhibition may represent a new therapeutic approach in PAH.
2023-01-20 | GSE200821 | GEO