Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide analysis of human pulmonary artery endothelial cells after knockdown of either BMPRII or beta-catenin

ABSTRACT: Expression analysis of genes potentially regulated by BMPRII and beta-catenin. BMPRII has been linked as a genetic factor to the disease pulmonary arterial hypertension.

ORGANISM(S): Homo sapiens

PROVIDER: GSE18956 | GEO | 2010/11/06

SECONDARY ACCESSION(S): PRJNA120991

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Genome-wide analysis of human pulmonary artery endothelial cells after knockdown of either BMPRII or beta-catenin

Project description:Expression analysis of genes potentially regulated by BMPRII and beta-catenin. BMPRII has been linked as a genetic factor to the disease pulmonary arterial hypertension. Comparison of total mRNA obtained from human pulmonary artery endothelial cells treated with control, bone morphogentic protein receptor II, or beta-catenin siRNA

2010-11-06 | E-GEOD-18956 | biostudies-arrayexpress

SMAD1/5 binding pattern in human pulmonary arterial endothelial cells [ChIP-seq]

Project description:We showed that the BMPRII/ALK-1/SMAD/ATOH8 axis protects against the development of pulmonary arterial hypertension (PAH). We have performed ChIP-seq analyses to reveal the function of both SMAD and ATOH8.

2019-10-17 | GSE104682 | GEO

ChIP-chip of BMP2 or control treated human pulmonary artery endothelial cells with anti-beta-catenin or anti-ppar-gamma antibodies on promoter regions

Project description:Reduced bone morphogenetic protein receptor (BMPR)2 expression in patients with pulmonary arterial (PA) hypertension (PAH), can impair PA endothelial cell (EC) function. We now characterize, in human PAECs, a novel BMPR2-mediated transcriptionally active complex between peroxisome proliferator-activated receptor (PPAR) gamma and beta-catenin (BC), and show that disruption of this complex impairs BMP mediated HPAEC survival. Using whole genome wide ChIP-Chip promoter analysis we delineate PPARG-BC dependent transcription of target genes that include apelin. Comparison of ppar-gamma and beta-catenin occupancy on promoter regions from human pulmonary artery endothelial cells after either treatment with BMP2 or control. A total of 8 samples were created using NimbleGen human HG18 promoter arrays.

2011-05-25 | E-GEOD-29489 | biostudies-arrayexpress

Effects of BMPR2 Loss in Human Pulmonary Artery Endothelial Cells

Project description:Pulmonary arterial hypertension (PAH) is a fatal disease characterized by a proliferative endothelial cell phenotype, inflammation and pulmonary vascular remodeling. BMPR2 loss-of-function has been linked to pathologic plexiform lesions with obliteration of distal pulmonary arteries distal pulmonary arteries BMPR2 silencing inprimary human pulmonary artery ECs (HPAECs) recapitulate important aspects of cellular dysfunction and deregulated signaling associated with PAH. Primary HPAECs were transfected with gene-specific siRNA pools targeting BMPR2 or control siRNA followed PMA or control stimulation.

2015-12-04 | E-GEOD-70456 | biostudies-arrayexpress

Effects of BMPR2 Loss in Human Pulmonary Artery Endothelial Cells

2015-12-04 | GSE70456 | GEO

ChIP-chip of BMP2 or control treated human pulmonary artery endothelial cells with anti-beta-catenin or anti-ppar-gamma antibodies on promoter regions

2011-05-25 | GSE29489 | GEO

Analysis of Differentially Regulated Genes in Lung Tissue

Project description:Pulmonary arterial hypertension (PAH) is a progressive fatal disease that is characterized by pathological pulmonary artery remodeling, in which endothelial cell (EC) dysfunction is critically involved. We herein describe a previously unknown role of endothelial angiocrine in pulmonary hypertension. By searching for genes highly expressed in lung microvascular ECs, we identified inhibin--A (INHBA) as an angiocrine factor produced by pulmonary capillaries. We found that excess production of INHBA by ECs impairs the endothelial function in an autocrine manner by functioning as activin A (ActA). Mechanistically, ActA induces bone morphogenetic protein receptor type 2 (BMPRII) internalization and targeting to lysosomes for degradation, resulting in BMPRII signal deficiency in ECs. When endothelial ActA-BMPRII link is overdriven in mice, hypoxia-induced pulmonary hypertension was exacerbated, whereas conditional knockout of INHBA in ECs prevents the progression of pulmonary hypertension. These data collectively indicate a critical role for the dysregulated endothelial ActA-BMPRII link in the progression of pulmonary hypertension, and thus endothelial INHBA/ActA is an attractive pharmacotherapeutic target for the treatment of PAH.

2020-12-15 | GSE156233 | GEO

Analysis of Differentially Regulated Genes in Lung Microvasculature

2020-12-15 | GSE156225 | 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

Transcriptomics and proteomics revealed sex differences in human pulmonary microvascular endothelial cells

Project description:There is marked sexual dimorphism displayed in the onset and progression of pulmonary hypertension (PH). Females more commonly develop pulmonary arterial hypertension (PAH), however, females with PAH and other types of PH have better survival than males. Pulmonary microvascular endothelial cells play a crucial role in the pulmonary vascular remodelling and increased pulmonary vascular resistance of PH. Given this background, we hypothesized that there are sex differences in the pulmonary microvascular endothelium basally and in response to hypoxia that are independent of the sex hormone environment.

2024-01-03 | PXD046787 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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