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Expression data analysis in lungs from mice induced for pulmonary arterial hypertension (PAH) by inhalation of Stachybotrys chartarum spores

ABSTRACT: It has been reported that repeated intra-tracheal instillation of S. chartarum spores induced significant pulmonary arterial remodeling in mice, which resulted in pathological changes like human pulmonary arterial hypertension (PAH) and elevation right ventricle systolic pressure. Then, we used microarrays to know the complex molecular mechanisms that underlie pathogenesis of PAH. Isolates of Stachybotrys chartarum were used. Ddy mice were anesthetized and the spore suspension was intratracheally injected 12 times, i.e. 1×104 spores into each mouse at 4-5 day intervals for 8 weeks. Mice were sacrificed one week after the final injection and then examined. Lung tissue specimens from mice model of PAH (n=3) and normal controls (n=3) were obtained. RNA targets preparation were performed according to the manufacturer's protocol using GeneChip(R) 3' IVT Express Kit (Affymetrix). One hundred nanograms of total RNA was converted into double-stranded cDNA template for transcription. In vitro transcription synthesized amplified RNA (aRNA) and incorporated a biotin-conjugated nucleotide. After purification and fragmentation of aRNA, 12.5 ug of them was hybridized to GeneChip(R) Mouse Genome 430 2.0 Array (Affymetrix).The Probe Array was scanned using a GeneChip(R) Scanner 3000 7G.

ORGANISM(S): Mus musculus

SUBMITTER: kayoko shimodaira

PROVIDER: E-GEOD-23178 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data analysis in lungs from mice induced for pulmonary arterial hypertension (PAH) by inhalation of Stachybotrys chartarum spores

Project description:It has been reported that repeated intra-tracheal instillation of S. chartarum spores induced significant pulmonary arterial remodeling in mice, which resulted in pathological changes like human pulmonary arterial hypertension (PAH) and elevation right ventricle systolic pressure. Then, we used microarrays to know the complex molecular mechanisms that underlie pathogenesis of PAH.

2010-07-29 | GSE23178 | GEO

Identification of Transcriptional markers in Peripheral Blood of Idiopathic PAH Patients

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2020-01-18 | E-MTAB-3276 | biostudies-arrayexpress

Pharmacological inhibition of G9a ameliorates pulmonary vascular remodeling in PAH

Project description:Background:Pulmonary arterial hypertension (PAH) is a severe condition characterized by progressive vascular remodeling of small pulmonary arteries (PAs) causing sustained elevation of PA pressure, right ventricular failure and death. Similar to cancer cells, PA smooth muscle cells (PASMCs), which play a key role in pulmonary vascular remodeling, have adopted multiple mechanisms to sustain their survival and proliferation in the presence of stress. The histone methyltransferase G9a has been shown to exert oncogenic effects and to serve as a buffer against an exaggerated transcriptional response. Therefore, we hypothesized that G9a up-regulation in PAH plays a pivotal role in pulmonary vascular remodeling by maintaining the abnormal phenotype of PAH-PASMCs. Methods: G9alevels were measured in PAs and isolated PASMCs of PAH patients and animal models. Selective G9a pharmacological inhibitors were used in human PAH-PASMCs and in rodent PAH models (i.e.Fawn-Hooded rats and Sugen/Hypoxia-exposed mice). Results: We present evidence of increased expression of G9a in PASMCs from PAH patients as well as in remodeled PAs from animal models. We found that pharmacological inhibition of G9a activity using BIX01294 and UNC0642significantly reduces the prosurvival and proproliferative potentials of cultured PAH-PASMCs. Using RNA sequencing, further exploration revealed that G9a promotes extracellular matrix production and affords protection against the negative effects of an overactive stress response. Finally, we found that therapeutic treatment with BIX01294 reduced pulmonary vascular remodeling and lowered mean PA pressure in Fawn-Hooded rats. Treatment of Sugen/hypoxia-challenged mice with BIX01294 also improved pulmonary hemodynamics and right ventricular function. Conclusions:These findings suggest that G9a inhibition may represent a new therapeutic approach in PAH.

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Limited systemic sclerosis patients with PAH show biomarkers of inflammation and vascular injury

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RNA Expression Profiling of Lung Tissue Identifies Mutually Distinct Molecular Signatures in PAH and PH Secondary to IPF

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2010-01-22 | GSE15197 | GEO

Limited systemic sclerosis patients with PAH show biomarkers of inflammation and vascular injury

2010-10-27 | GSE19617 | GEO

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2024-09-27 | PXD055773 | JPOST Repository

Bmpr2 mutation in murine PMVEC

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