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Links from GEO DataSets

Items: 20

1.
Full record GDS4543

Pulmonary vascular microendothelial cell response to mutations in type 2 receptor for the bone morphogenetic protein signaling pathway, BMPR2

Analysis of PMVECs cultured from triple transgenics carrying immortomouse gene, a transactivator, and either control, Bmpr2delx4+ or Bmpr2R899X mutation. Hereditary pulmonary arterial hypertension is often associated with BMPR2 mutations. Results provide insight into role of Bmpr2 in endothelium.
Organism:
Mus musculus
Type:
Expression profiling by array, transformed count, 3 genotype/variation sets
Platform:
GPL6246
Series:
GSE28043
6 Samples
Download data: CEL
2.

Bmpr2 mutation in murine PMVEC

(Submitter supplied) Pulmonary arterial hypertension (PAH) is thought to be driven by dysfunction of pulmonary vascular microendothelial cells (PMVEC). Most hereditary PAH is associated with BMPR2 mutations. However, the physiologic and molecular consequences of expression of BMPR2 mutations in PMVEC are unknown.
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS4543
Platform:
GPL6246
6 Samples
Download data: CEL
Series
Accession:
GSE28043
ID:
200028043
3.

Effects of ACE2 on BMPR2 mutation-mediated defects in gene expression

(Submitter supplied) BMPR2 mutation causes pulmonary arterial hypertension (PAH); ACE2 treatment can resolve established BMPR2-mediated PAH. The purpose of this study was to uncover the molecular mechanism behind this.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
8 Samples
Download data: CEL, CHP
Series
Accession:
GSE21583
ID:
200021583
4.

Effect of BMPR2-R899X mutation in lung with and without elevated RVSP

(Submitter supplied) Familial pulmonary arterial hypertension (fPAH) is associated with mutations in BMPR2. Many of these mutations occur in the BMPR2 tail domain, leaving the SMAD functions intact. In order to determine the in vivo consequences of BMPR2 tail domain mutation, we created a smooth-muscle specific doxycycline inducible BMPR2 mutation with an arginine to termination mutation at amino acid 899. When these SM22-rtTA x TetO7-BMPR2R899X mice had transgene induced for 9 weeks, starting at 4 weeks of age, they universally developed pulmonary vascular pruning as assessed by fluorescent microangiography. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS3799
Platform:
GPL1261
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE11018
ID:
200011018
5.
Full record GDS3799

Bone morphogenetic protein type II receptor mutation effect on lung

Analysis of lung from transgenics expressing a BMPR2 tail domain mutation (BMPR2R899X) in smooth muscle. Nine weeks of BMPR2R899X expression can result in elevated right ventricular systolic pressures (RVSP), producing a mutant phenotype relevant to human pulmonary arterial hypertension (PAH).
Organism:
Mus musculus
Type:
Expression profiling by array, count, 3 disease state sets
Platform:
GPL1261
Series:
GSE11018
6 Samples
Download data: CEL, CHP
6.

Effects of BMPR2 Loss in Human Pulmonary Artery Endothelial Cells

(Submitter supplied) 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.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL15207
16 Samples
Download data: CEL
Series
Accession:
GSE70456
ID:
200070456
7.

Human pulmonary artery endothelial cells (hPAECs) with downregulated BMPR2 signaling demonstrate a unique gene expression signature after exposure to overexpression of AdAlox5

(Submitter supplied) Bmpr2 mutations are critical risk factors for hereditary pulmonary arterial hypertension (hPAH) with approximately 20% of carriers developing disease. There is an unmet medical need to understand how environmental factors, such as inflammation, render Bmpr2 mutants susceptible to PAH. Overexpressing 5-lipoxygenase (5-LO) provokes lung inflammation and transient PAH in Bmpr2+/- mice. Accordingly, 5-LO and its metabolite, leukotriene B4 (LTB4), are candidates for the ‘second hit’. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
18 Samples
Download data: TXT
8.

Loss of BMPR2 Signaling in Smooth Muscle in Mouse Lung

(Submitter supplied) Mice expressing a doxycycline-inducible dominant negative BMPR2 transgene expressed only in smooth muscle are activated for one or eight weeks, and compared to transactivator-only mice also fed doxycycline. All mice are 12 weeks of old at sacrifice. Keywords: time course with SM22-rtTA x tetO7-BMPR2 transgene
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS2147
Platform:
GPL1261
6 Samples
Download data
Series
Accession:
GSE5255
ID:
200005255
9.
Full record GDS2147

Bone morphogenic protein receptor 2 inactivation in smooth muscle effect on the lung: time course

Analysis of lungs 1 or 8 weeks following induction in smooth muscle of a dominant negative mutant form of type 2 bone morphogenic protein receptor (BMPR2). Results provide insight into the pathogenesis of hereditary pulmonary arterial hypertension (PAH), a disorder associated with BMPR2 mutations.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 gender, 2 genotype/variation, 2 time sets
Platform:
GPL1261
Series:
GSE5255
6 Samples
Download data
DataSet
Accession:
GDS2147
ID:
2147
10.

Glucose metabolism induced chromatin remodeling in pulmonary artery endothelial cell

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL20301
22 Samples
Download data
Series
Accession:
GSE89788
ID:
200089788
11.

Glucose metabolism induced chromatin remodeling in pulmonary artery endothelial cell [RNA-Seq]

(Submitter supplied) Maintaining endothelial cells (EC) as a monolayer in the vessel wall depends on a gene expression profile and the metabolic state, features influenced by contact with neighboring cells eg, pericytes and smooth muscle cells (SMC). Dysfunctional bone morphogenetic protein receptor 2 (BMPR2) signaling disrupts EC metabolism and monolayer formation and is associated with vascular diseases such as pulmonary arterial hypertension. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
2 Samples
Download data: DIFF
12.

Glucose metabolism induced chromatin remodeling in pulmonary artery endothelial cell [ChIP-Seq]

(Submitter supplied) Maintaining endothelial cells (EC) as a monolayer in the vessel wall depends on a gene expression profile and the metabolic state, features influenced by contact with neighboring cells eg, pericytes and smooth muscle cells (SMC). Dysfunctional bone morphogenetic protein receptor 2 (BMPR2) signaling disrupts EC metabolism and monolayer formation and is associated with vascular diseases such as pulmonary arterial hypertension. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
20 Samples
Download data: TXT
Series
Accession:
GSE89786
ID:
200089786
13.

P53-dependent Genes in Human Pulmonary Smooth Muscle Cells

(Submitter supplied) We report differentially expressed genes in human pulmonary arterial smooth muscle cells under genotoxic stress (Doxorubicin) or pharmacological p53-activation by Nutlin-3.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
6 Samples
Download data: TXT
14.

Genome-wide mapping of p53-binding in 293T cells

(Submitter supplied) We report p53-target genes in response to DNA damage in 293T cells
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
8 Samples
Download data: TXT
Series
Accession:
GSE154103
ID:
200154103
15.

P53-dependent Genes in Human Pulmonary Adventitial Fibroblasts

(Submitter supplied) We report differentially expressed genes in human pulmonary arterial adventitial fibroblasts under genotoxic stress (Doxorubicin) or pharmacological p53-activation by Nutlin-3.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
6 Samples
Download data: TXT
16.

Genome-wide mapping of p53-transcriptional activity in the pulmonary endothelium

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
20 Samples
Download data: BED, TXT
Series
Accession:
GSE139863
ID:
200139863
17.

Genome-wide mapping of p53-transcriptional activity in the pulmonary endothelium [RNA-seq]

(Submitter supplied) We report a pharmacologically inducible vasculoprotective mechanism in pulmonary arterial endothelial cells (PAEC) in response to DNA damage by p53 and a novel PPARgamma/p53 transcription factor complex.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
12 Samples
Download data: TXT
18.

Genome-wide mapping of p53-transcriptional activity in the pulmonary endothelium [ChIP-seq]

(Submitter supplied) We report a pharmacologically inducible vasculoprotective mechanism in pulmonary arterial endothelial cells (PAEC) in response to DNA damage by p53 and a novel PPARgamma/p53 transcription factor complex.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
8 Samples
Download data: BED, TXT
Series
Accession:
GSE139858
ID:
200139858
19.

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

(Submitter supplied) 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.
Organism:
Rattus norvegicus
Type:
Expression profiling by array
Platform:
GPL14797
8 Samples
Download data: TXT
Series
Accession:
GSE42767
ID:
200042767
20.

iPSCs Reveal Protective Modifiers of the BMPR2 mutation in Pulmonary Arterial Hypertension

(Submitter supplied) The goal of this study is to compare transcriptome profiling (RNA-seq) in controls, unaffected BMPR2 mutation carriers and affected familial pulmonary arterial hypertension patients, to elucidate a protective feature in iPS derived endothelial cells from the mutation carriers.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
11 Samples
Download data: TXT
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