GEO DataSets

(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

(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

(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

(Submitter supplied) Tissue Factor Pathway Inhibitor-2 is Induced by Fluid Shear Stress in Vascular Smooth Muscle Cells and Affects Cell Proliferation and Survival Introduction: Vascular smooth muscle cells (SMCs) are exposed to fluid shear stress (FSS) after interventional procedures such as balloon-angioplasty. Whereas the effects of hemodynamic forces on endothelial cells are explored in detail, the influence of FSS on smooth muscle cell function is poorly characterized. more...

Organism:

Rattus norvegicus

Type:

Expression profiling by array

Platform:

GPL1355

6 Samples

Download data: CEL

(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

(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

(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

(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

(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

(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

(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

(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

(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

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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

(Submitter supplied) Laminar flow on endothelial cells in vitro activates MEF2 transcription factors to induce expression of atheroprotective genes. Here we sought to establish in vivo MEF2 functions in the endothelium through endothelial-specific deletion of Mef2c. Our results show that endothelial Mef2c regulates migration of vascular smooth muscle from the tunica media into the intima through fenestrations in the internal elastic lamina. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL20775

8 Samples

Download data: CEL, CHP

(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

(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

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

(Submitter supplied) The goal of this study is to identify the target of PAH in PASMC from donor control and PAH patients by transcriptome profiling (RNA-seq) and the mechanism from transcriptome profiling (RNA-seq) and histone modification (ChIPseq)

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL16791

39 Samples

Download data: TXT

(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