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Gene expression profile at single cell level of cells in distal pulmonary arteries from healthy and hypoxia-induced pulmonary hypertensive calves

ABSTRACT: Gene expression profile at single cell level of cells in distal pulmonary arteries from healthy and hypoxia-induced pulmonary hypertensive calves

PROVIDER: PRJNA980212 | ENA |

REPOSITORIES: ENA

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Gene expression profile at single cell level of cells in distal pulmonary arteries from healthy and hypoxia-induced pulmonary hypertensive calves

Project description:Distal pulmonary arteries contain multipe cell types and each cell type contains multiple functional state. We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of cell types in control animals and the changes of cell types and gene expression between cells from healthy and PH vessels.

2023-07-10 | GSE234156 | GEO

Comparing CTEPH to Control and IPAH pulmonary arteries

Project description:Samples surgically extracted from CTEPH pulmonary arteries were compared to post-transplant pulmonary arteries from IPAH and failed donor pulmonary arteries from controls The goal was to determine if altered gene expression in CTEPH associated with development of chronic thrombi

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Hypoxia Induced Pulmonary Hypertension

Project description:Here we investigated the protein composition of the main pulmonary artery (MPA), distal pulmonary arteries (DPA) distal whole lung (DWL) of early stage hypoxia (using a neonatal bovine calf model) and late stage hypoxia (using adult steers with hypoxia-induced PH) using high resolution mass spectrometry. Compartment-resolved analysis allowed for quantitative measurements of proteins from cellular, soluble ECM and insoluble ECM fractions

2022-10-06 | MSV000090482 | MassIVE

Effect of pulmonary hypertension due to left heart disease on gene expression in pulmonary arteries

Project description:Pulmonary hypertension worsens outcome in left heart disease. Stiffening of the pulmonary artery may drive this pathology by increasing right ventricular dysfunction and lung vascular remodeling. We showed that pulmonary arteries from patients with left heart disease are characterized by increased stiffness that correlates with impaired pulmonary hemodynamics. Pulmonary arteries in left heart disease patients with pulmonary hypertension were characterized by degradation of elastic fibers paralleled by an accumulation of fibrillar collagens. We utilized RNA sequencing to identify differentially expressed genes regulating extracellular matrix remodeling in pulmonary arteries of left heart disease patients with or without pulmonary hypertension, in comparison to healthy-heart donor controls. As such we identified that transcriptional deregulation of extracellular matrix constituents and their regulators precedes clinical pulmonary hypertension, and therefore might be a pathomechanism that drives pulmonary arterial remodeling and stiffening in left heart disease.

2023-07-03 | GSE236251 | GEO

Differential proteomics - Pulmonary pressure reduction attenuates expression of proteins identified by lung proteomic profiling in pulmonary hypertensive rats

Project description:Pulmonary pressure reduction attenuates expression of proteins identified by lung proteomic profiling in pulmonary hypertensive rats

2011-09-28 | PRD000524 | Pride

Genome wide gene expression profiling in the pulmonary arteries; role of the serotonin transporter Gender and Hypoxia

Project description:Genome-wide gene expression profiling was performed in pulmonary arteries from 32 mice. Four mice in 8 different groups; Normoxic: wild type female/male, Sert female/male; Hypoxic: wild type female/male and Sert female/male.

2010-12-16 | E-MTAB-455 | biostudies-arrayexpress

RNAseq of perivascular adipose tissue from mesenteric arteries from normotensive and hypertensive Dahl S rats

Project description:We report the results from RNA-seq analysis of perivascular adipose tissues (PVAT) collected from mesenteric arteries from Dahl S rats. Animals were on a control or a high fat diet for 24 weeks. At the moment of collection, rats fed high fat diet were hypertensive. In contrast, rats on the control diet were normotensive.

2021-01-23 | GSE165369 | GEO

Comparing CTEPH to Control and IPAH pulmonary arteries

Project description:Comparing CTEPH to Control and IPAH pulmonary arteries

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Transcription profiling of rat arteries from animals with salt induced hypertensive disease results in over expression of matricellular genes in cerebral arteries

Project description:The Dahl salt-sensitive (S) rat model develops chronic hypertensive disease when fed a high salt diet that ultimately results in renal and heart failure, as well as prevalent cerebrovascular pathologies. Phenotypic changes in the cerebral vasculature are preceded by changes in gene expression, and evidence supports a role for extracellular signal-regulated kinase 1/2 (ERK1/2) in vascular cell proliferation, yet little is known regarding ERK1/2 âregulated gene transcription in cerebrovascular smooth muscle during hypertension. Findings presented here support the hypothesis that salt-induced hypertensive disease results in upregulation of ERK1/2 activity and ERK1/2-regulated genes that promote remodeling in cerebral resistance arteries. Dahl S rats were fed either a 0.4% NaCl (low salt, LS) or 8% NaCl (high salt, HS) diet until evidence of left ventricular dysfunction. Gene expression profiling using oligonucleotide array analysis detected a significant fold-change of 1.5 or greater in 133 out of 15,923 genes examined. Mitogen-activated protein kinase (MAPK)-regulated genes were overrepresented and provided a link to genes involved in proliferation and extracellular matrix signaling including plasminogen activator inhibitor I (PAI-1), osteopontin (OPN) and junB. These data suggests that salt induced hypertensive disease promotes hyperplasia and changes in matricellular genes that are likely important in vascular remodeling. Experiment Overall Design: Analysis was based on a comparison between the Low Salt and High Salt groups. Arteries from 3 animals were pooled for each sample, thus there were 9 animals/group. Analysis of significance amongst all genes as well as prospective hypotheses correlating to disease were performed.

2008-06-13 | E-GEOD-5488 | biostudies-arrayexpress

Salt Induced Hypertensive Disease Results in Over Expression of Matricellular Genes in Cerebral Arteries

Project description:The Dahl salt-sensitive (S) rat model develops chronic hypertensive disease when fed a high salt diet that ultimately results in renal and heart failure, as well as prevalent cerebrovascular pathologies. Phenotypic changes in the cerebral vasculature are preceded by changes in gene expression, and evidence supports a role for extracellular signal-regulated kinase 1/2 (ERK1/2) in vascular cell proliferation, yet little is known regarding ERK1/2 –regulated gene transcription in cerebrovascular smooth muscle during hypertension. Findings presented here support the hypothesis that salt-induced hypertensive disease results in upregulation of ERK1/2 activity and ERK1/2-regulated genes that promote remodeling in cerebral resistance arteries. Dahl S rats were fed either a 0.4% NaCl (low salt, LS) or 8% NaCl (high salt, HS) diet until evidence of left ventricular dysfunction. Gene expression profiling using oligonucleotide array analysis detected a significant fold-change of 1.5 or greater in 133 out of 15,923 genes examined. Mitogen-activated protein kinase (MAPK)-regulated genes were overrepresented and provided a link to genes involved in proliferation and extracellular matrix signaling including plasminogen activator inhibitor I (PAI-1), osteopontin (OPN) and junB. These data suggests that salt induced hypertensive disease promotes hyperplasia and changes in matricellular genes that are likely important in vascular remodeling. Keywords: Normotensive vs. Hypertensive Disease

2007-08-09 | GSE5488 | GEO

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