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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of whole lungs from mice expressing an inducible dominant negative BMPR2 transgene to study the effect of BMPR2 on gene expression.

ABSTRACT: 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. Experiment Overall Design: Each chip is a pool of three individual mice, to reduce variability. The transactivator-only mice are controls. The other mice all had elevated RV pressures at time of sacrifice. RNA was prepared from whole lung.

ORGANISM(S): Mus musculus

SUBMITTER: James West

PROVIDER: E-GEOD-5255 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Molecular effects of loss of BMPR2 signaling in smooth muscle in a transgenic mouse model of PAH.

Tada Yuji Y Majka Susan S Carr Michelle M Harral Julie J Crona Daniel D Kuriyama Takayuki T West James J

American journal of physiology. Lung cellular and molecular physiology 20070316 6

Idiopathic pulmonary arterial hypertension (IPAH) in human patients is associated with mutations in type 2 receptor for the bone morphogenic protein pathway (BMPR2). Mice expressing an inducible dominant negative form of BMPR2 in smooth muscle develop elevated right ventricular pressures when the transgene is activated. We hypothesized that transcriptional changes in these mice may allow insight into the early molecular events leading to IPAH. Microarray analysis was used to examine the transcri ...[more]

PMID: 17369292

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Loss of BMPR2 Signaling in Smooth Muscle in Mouse Lung

Project description: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

2006-07-08 | GSE5255 | GEO

Transcription profiling of mouse inducible BMPR2 mutant vs. controls in lung with and without elevated RVSP

Project description: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. Approximately half the time the induced animals developed elevated right ventricular systolic pressures (RVSP), associated with extensive pruning, muscularization of small pulmonary vessels, and development of large structural pulmonary vascular changes. These lesions included large numbers of macrophages and T-cells in their adventitial compartment, as well as CD133 positive cells in the lumen. Small vessels filled with CD45 positive and sometimes CD3 positive cells were a common feature in all SM22-rtTA x TetO7-BMPR2R899X mice. Gene array experiments show changes in stress response, muscle organization and function, proliferation and apoptosis, and developmental pathways before RVSP increases. Our results show that the primary phenotypic result of BMPR2 tail domain mutation in smooth muscle is pulmonary vascular pruning leading to elevated RVSP, associated with early dysregulation in multiple pathways with clear relevance to PAH. This model should be useful to the research community in examining early molecular and physical events in the development of PAH, and as a platform to validate potential treatments. Experiment Overall Design: Each array is an individual female mouse, age-matched, with two mice & arrays used for each of controls (transactivator only), BMPR2-R899X with normal RVSP, and BMPR2-R899X with high RVSP.

2008-06-18 | E-GEOD-11018 | biostudies-arrayexpress

Bmpr2 mutation in murine PMVEC

Project description: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. PMVEC were isolated from triple transgenic mice carrying the immortomouse gene, a transactivator, and either control, Bmpr2delx4+ or Bmpr2R899X mutation

2011-07-01 | E-GEOD-28043 | biostudies-arrayexpress

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

2008-06-01 | GSE11018 | GEO

RNASeq of adipocytes from ROSA vs BMPR2 DELX mice

Project description:We sequenced RNA from adipocytes of ROSA and BMPR2 DELX transgenic mice

2019-02-18 | GSE94784 | GEO

Bmpr2 mutation in murine PMVEC

2011-07-01 | GSE28043 | GEO

Effect of BMPR2 mutation on vascular smooth muscle gene expression

Project description:BMPR2 mutation is the cause of most hereditary pulmonary arterial hypertension, but the common molecular consequence of different types of BMPR2 mutation is still not known. The goal of this study was to determine the common molecular consequences of three different classes of patient-derived BMPR2 mutation in vascular smooth muscle gene expression. Three different classes of BMPR2 mutation, wild-type BMPR2, or empty vector were stably transfected into A7R5 vascular smooth muscle cells, and expression compared.

2010-08-25 | E-GEOD-21573 | biostudies-arrayexpress

Effect of BMPR2 mutation on vascular smooth muscle gene expression

2010-08-25 | GSE21573 | GEO

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

Project description: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. Four groups: +/- ACE2 and +/- BMPR2 transgene, two arrays each, each array a pool of three animals.

2010-08-24 | E-GEOD-21583 | biostudies-arrayexpress

BMPR2 Regulates Hypoxic Extracellular Vesicle Signaling to Maintain Vascular Homeostasis.

Project description:To investiage the BMPR2 dependent effects of extracellular vesicle (EV) treatment, we compared the miRNA composition of EV derived from pulmonary arteerial endothelial cells after BMPR2 knockdown and 24 hours hypoxia.

2023-05-10 | GSE202648 | GEO

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