Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-cigarettes induce dysregulation of autophagy leading to endothelial dysfunction in pulmonary arterial hypertension

ABSTRACT: To investigate whether differential susceptibility exists between healthy and PAH patients to e-cig exposure and the molecular mechanisms, human iPSC lines from two healthy volunteers and two FPAH patients were first differentiated into ECs. iPSC-ECs were then treated with and without e-cigarette extract for 24 hours.

ORGANISM(S): Homo sapiens

PROVIDER: GSE199764 | GEO | 2025/03/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-seq of iPSC-ECs treated e-cig liquids with and without nicotine

Project description:Two healthy iPSC lines (78 and 273) were differentiated into ECs. iPSC-ECs were then treated with e-cig liquids RY4 (RY) or Marcado (MAR) with 18mg/ml of nicotine (18) and without nicotine (0).

2020-08-11 | GSE125217 | GEO

miRNA array of patients with Pulmonary Arterial Hypertension

Project description:Comparison of miRNA expression between patients with idiopathic and systemic sclerosis PAH and healthy controls and systemic sclerosis without PAH

2021-06-01 | E-MTAB-10425 | biostudies-arrayexpress

lncRNA Array of iPSC-ECs treated with and without e-cigarette extraction

Project description:Four healthy iPSC lines were differentiated into ECs. iPSC-ECs were then treated with and without e-cigarette extraction for 24 hours.

2024-10-16 | GSE186227 | GEO

Investigation of endothelial cell gene dysregulation in early pulmonary arterial hypertension disease model

Project description:Endothelial cell (EC) dysfunction plays a key role in the pathogenesis of pulmonary arterial hypertension (PAH). To avoid cell cultures and whole lung tissue samples, we have, for the first time, used CD31 antibody coated magnetic beads in conjunction with genome scale RNA expression microarrays to profile ECs in vivo at any stage of PAH. We hypothesized that targeting early stages of the disease would identify novel mediators of PAH and genes linked to bone morphogenetic protein receptor 2 (BMPR2) signaling. Rats were treated with either monocrotaline (60mg/kg) or saline as control with 4 animals in each experimental group. Gene expression profiling was performed on primary pulmonary endothelial cells directly after isolation from whole lung tissue 5 days after treatment.

2014-02-06 | E-GEOD-42767 | biostudies-arrayexpress

Investigation of endothelial cell gene dysregulation in early pulmonary arterial hypertension disease model

2014-02-06 | GSE42767 | 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

Metabolomic heterogeneity of severe pulmonary arterial hypertension

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

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

Metabolomic heterogeneity of severe pulmonary arterial hypertension

2014-11-14 | GSE53408 | GEO

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data