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Links from GEO DataSets

Items: 11

1.
Full record GDS5610

Heritable pulmonary arterial hypertension: cardiac right ventricular wall

Analysis of biopsies of right ventricle (RV) from patients with pulmonary arterial hypertension (PAH) with bone morphogenetic protein receptor type II (BMPR2) mutation. Results provide insight into molecular mechanisms underlying the metabolic effects of mutant BMPR2 in PAH RVs.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 3 disease state sets
Platform:
GPL6244
Series:
GSE67492
6 Samples
Download data: CEL
2.

Expression data from human heart right ventricular wall

(Submitter supplied) Gene expression in the right ventricle is different in control patients as compared to either idiopathic dilated cardiomyopathy or pulmonary arterial hypertension
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5610
Platform:
GPL6244
6 Samples
Download data: CEL
Series
Accession:
GSE67492
ID:
200067492
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.

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
7.
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
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.

Rabbit heart gene expression in Left ventricle (LV) following banding of the descending thoracic aorta (AOB-LV) vs Sham-control LV and in Right ventricle (RV) following banding the pulmonary artery (PAB-RV) vs. Sham-control RV

(Submitter supplied) Background: Right ventricular (RV) and left ventricular (LV) myocardium differ in their response to pressure-overload hypertrophy (POH). In this report we use microarray and proteomic analyses to identify pathways modulated by LV-, and RV-POH in the immature heart. Methods: Newborn New Zealand White rabbits underwent banding of the descending thoracic aorta (LV-POH; n=6). RV-POH was achieved by banding the pulmonary artery (n=6). more...
Organism:
Oryctolagus cuniculus
Type:
Expression profiling by array
Platform:
GPL13758
6 Samples
Download data: GPR
Series
Accession:
GSE30194
ID:
200030194
11.

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
Series
Accession:
GSE133749
ID:
200133749
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