Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Human_IPAH_LMM_Arteries

ABSTRACT: Idiopathic pulmonary arterial hypertension (iPAH) is a fatal disease that is associated with increased vascular resistance due to sustained contraction and enhanced proliferation of pulmonary vascular cells. The current treatment however is still not satisfactory. A better understanding of the involved molecular mechanisms may lead to new therapeutical strategies. Pulmonary arterial walls of healthy human lung tissue and of iPAH lungs were laser-microdissected. The extracted RNA was pooled and subjected to SMART-based RNA preamplification and fluorescence labeling. Gene expressions between iPAH and donors were compared using dual-channel microarrays. Keywords: disease characterization

ORGANISM(S): Homo sapiens

PROVIDER: GSE10704 | GEO | 2008/11/21

SECONDARY ACCESSION(S): PRJNA107581

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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.

2024-04-04 | GSE256539 | GEO

Identifying microRNAs targeting WNT/β-catenin pathway in end-stage idiopathic pulmonary arterial hypertension

Project description:Whole genome microRNA microarray expression profiling was employed as a discovery platform to identify microRNAs dysregulated in end-stage idiopathic pulmonary arterial hypertension (IPAH) patients. Lung tissue from seven IPAH patients and eight failed donor controls were subjected to microarray screening. Twenty-one miRNAs were identified dyeregulated in IPAH patients compared to controls. In miRNA real-time PCR validation, 22 IPAH patients and 22 control subjects were enrolled, including the 7 IPAH and 8 controls in microarray screening. Expression levels of five miRNAs (let-7a-5p, miR-199a-3p, miR-199b-5p, miR-26b-5p and miR-27b-3p) were upregulated in technical validation. Tissue miRNA levels had positive correlation with pulmonary vascular remodeling and hemodynamic changes in IPAH patients compared to controls.

2017-08-23 | GSE67597 | GEO

Molecular changes implicate angiogenesis and arterial remodeling in systemic sclerosis-associated and idiopathic pulmonary hypertension

Project description:Pulmonary hypertension (PH) is a common complication of systemic sclerosis (SSc) and a leading cause of mortality among patients with this disease. PH can also occur as an idiopathic condition (idiopathic pulmonary arterial hypertension, iPAH). We sought to investigate the transcriptomic alterations in PH vascular populations to understand cellular mechanisms underlying pathobiology of systemic sclerosis associated and idiopathic pulmonary hypertension.

2024-06-07 | GSE244781 | GEO

human lung metagenome

Project description:IPAH (Idiopathic Pulmonary Arterial Hypertension) Metagenome

| PRJNA279445 | ENA

Endothelial senescence mediates hypoxia-induced vascular remodeling by modulating PDGFB expression

Project description:Uncontrolled accumulation of pulmonary artery smooth muscle cells (PASMC) to the distal pulmonary arterioles (PAs) is one of the major characteristics of pulmonary hypertension (PH). Cellular senescence contributes to aging and lung diseases associated with PH and links to PH progression. However, the mechanism by which cellular senescence controls vascular remodeling in PH is not fully understood. The levels of senescence marker, p16INK4A and senescence-associated β-galactosidase (SA-β-gal) activity are higher in PA endothelial cells (ECs) isolated from idiopathic pulmonary arterial hypertension (IPAH) patients compared to those from healthy individuals. Hypoxia-induced accumulation of α-smooth muscle actin (αSMA)-positive cells to the PAs is attenuated in p16fl/fl-Cdh5(PAC)-CreERT2 (p16iΔEC) mice after tamoxifen induction. We have reported that endothelial TWIST1 mediates hypoxia-induced vascular remodeling by increasing platelet-derived growth factor (PDGFB) expression. Transcriptomic analyses of IPAH patient or hypoxia-induced mouse lung ECs reveal the alteration of senescence-related gene expression and their interaction with TWIST1. Knockdown of p16INK4A attenuates the expression of PDGFB and TWIST1 in IPAH patient PAECs or hypoxia-treated mouse lungs and suppresses accumulation of αSMA–positive cells to the supplemented ECs in the gel implanted on the mouse lungs. Hypoxia-treated mouse lung EC-derived exosomes stimulate DNA synthesis and migration of PASMCs in vitro and in the gel implanted on the mouse lungs, while p16iΔEC mouse lung EC-derived exosomes inhibit the effects. These results suggest that endothelial senescence controls αSMA–positive cell proliferation and migration in PH through TWIST1-PDGFB signaling.

2022-10-15 | PXD033549 | Pride

Transcription profiling of human normal subjects and IPAH patients to examine the effect of BMP-2 on pulmonary artery smooth muscle cells

Project description:Bone morphogenetic proteins (BMP) inhibit proliferation and induce apoptosis in pulmonary artery smooth muscle cells (PASMC) from normal subjects. Dysfunction of BMP signaling due to mutations in and/or downregulation of BMP receptors has been implicated in idiopathic pulmonary arterial hypertension (IPAH). We examined whether BMP differentially regulates gene expression in PASMC from normal subjects and IPAH patients using the Affymetrix microarray analysis. BMP-2 treatment (200 nM for 24 hrs) altered expression levels of 6,206 genes in normal and IPAH PASMC. 1,063 of these genes were regulated oppositely by BMP-2: 523 genes were downregulated by BMP-2 in normal PASMC but upregulated in IPAH PASMC, whereas 540 genes were upregulated by BMP-2 in normal PASMC but downregulated in IPAH PASMC. The divergent effects of BMP-2 on gene expression profiles indicate that PASMC may undergo significant phenotypic changes in IPAH patients during development of the disease. The transition of the antiproliferative effect of BMP-2 in normal PASMC to its proliferative effect in IPAH patients is attributed potentially to its differential effect on expression patterns of various genes that are involved in cell proliferation and apoptosis. Among the 6206 BMP-2-sensitive genes, there are more than 1800 genes whose expression levels were negatively (with a correlation coefficient, r, < -0.9) or positively (with r > +0.9) correlated with the pulmonary arterial pressure. These results suggest that BMP-mediated gene regulation is significantly altered in PASMC from IPAH patients and mRNA expression changes in BMP-regulated genes may be involved in the development of IPAH.

2007-09-07 | E-GEOD-2559 | biostudies-arrayexpress

Fatty acid-binding proteins contribute to the pathogenesis of pulmonary hypertension [bulk RNA-seq]

Project description:Rationale: Pulmonary arterial hypertension (PAH) is a devastating disease characterized by obliterative vascular remodeling and persistent increase of vascular resistance, leading to right heart failure and premature death. Understanding the cellular and molecular mechanisms will help develop novel therapeutic approaches for PAH patients. Objectives: To determine whether upregulation of fatty-acid binding protein 4 and 5 (FABP4/5) is critical in pathogenesis of PAH. Methods: FABP4/5 expression was examined in pulmonary arterial endothelial cells (PAECs) and lung tissues from patients with idiopathic PAH and pulmonary hypertension (PH) rat models. Plasma proteome analysis was performed in human PAH samples. Echocardiography, hemodynamics, histology, and immunostaining were performed to evaluate the lung and heart PH phenotypes in Egln1Tie2Cre (CKO) mice and Egln1Tie2Cre/Fabp4-5-/- (TKO) mice. Measurement and Main Results: Both FABP4 and FABP5 were highly induced in ECs of CKO mice and PAECs from IPAH patients, and in whole lungs of PH rats. Plasma levels of FABP4/5 were upregulated in IPAH patients and directly correlated with severity of hemodynamics and biochemical parameters. Genetic deletion of both Fabp4 and 5 in CKO mice caused a reduction of right ventricular systolic pressure (RVSP) and RV hypertrophy, attenuated pulmonary vascular remodeling and prevented the right heart failure. Fabp4/5 deletion also normalized EC glycolysis, reduced ROS and HIF-2a expression, and decreased aberrant EC proliferation in CKO lungs. Conclusions: PH causes aberrant expression of FABP4/5 in pulmonary ECs which leads to enhanced EC glycolysis and hyperproliferation, contributing to the accumulation of arterial ECs and vascular remodeling and exacerbating the disease.

2024-08-02 | GSE261445 | GEO

RNA sequencing of healthy and diseased (idiopathic pulmonary hypertension) human pulmonary artery smooth muscle cells

Project description:We performed RNA-seq to analyze gene expression in human PASMCs (Pulmonary arterial smooth muscle cells) isolated from subjects without disease and from subjects with IPAH (idiopathic pulmonary hypertension)

2020-07-15 | GSE144274 | GEO

Effect of BMP-2 on Pulmonary Artery Smooth Muscle Cells from Patients with Idiopathic Pulmonary Arterial Hypertension

Project description:Bone morphogenetic proteins (BMP) inhibit proliferation and induce apoptosis in pulmonary artery smooth muscle cells (PASMC) from normal subjects. Dysfunction of BMP signaling due to mutations in and/or downregulation of BMP receptors has been implicated in idiopathic pulmonary arterial hypertension (IPAH). We examined whether BMP differentially regulates gene expression in PASMC from normal subjects and IPAH patients using the Affymetrix microarray analysis. BMP-2 treatment (200 nM for 24 hrs) altered expression levels of 6,206 genes in normal and IPAH PASMC. 1,063 of these genes were regulated oppositely by BMP-2: 523 genes were downregulated by BMP-2 in normal PASMC but upregulated in IPAH PASMC, whereas 540 genes were upregulated by BMP-2 in normal PASMC but downregulated in IPAH PASMC. The divergent effects of BMP-2 on gene expression profiles indicate that PASMC may undergo significant phenotypic changes in IPAH patients during development of the disease. The transition of the antiproliferative effect of BMP-2 in normal PASMC to its proliferative effect in IPAH patients is attributed potentially to its differential effect on expression patterns of various genes that are involved in cell proliferation and apoptosis. Among the 6206 BMP-2-sensitive genes, there are more than 1800 genes whose expression levels were negatively (with a correlation coefficient, r, < –0.9) or positively (with r > +0.9) correlated with the pulmonary arterial pressure. These results suggest that BMP-mediated gene regulation is significantly altered in PASMC from IPAH patients and mRNA expression changes in BMP-regulated genes may be involved in the development of IPAH. Keywords = bone morphogenetic receptor protein Keywords = idiopathic pulmonary arterial hypertension Keywords = transcription factor Keywords = gene expression profile Keywords: other

2005-10-21 | GSE2559 | GEO

Il13-stimulation of human paSMCs

Project description:Idiopathic pulmonary arterial hypertension (IPAH) is characterized by medial hypertrophy due to pulmonary arterial smooth muscle cell (paSMC) hyperplasia. Interleukin (IL)-13 is a potent regulator of tissue fibrosis and remodelling, and its effects are dependent on the cell-type specific expression of the IL-13 receptor isotypes IL-4RÎ±, IL-13RÎ±1, and IL-13RÎ±2. In order to identify the possible mechanism how IL-13 can exert its antiproliferative effect on paSMC microarray analysis was performed. For this purpose paSMC were stimulated with IL-13(10ng/ml) for 2h and 6h, respectively and subjected to microarray analysis. Comparison of stimulated versus unstimulated cells. 3 biological replicates, 2 time points

2010-05-07 | E-GEOD-15739 | 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