Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA85171 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Hypoxia can induce vasoconstriction followed by vascular remodeling including hypertrophy and hyperplasia of pulmonary vascular smooth muscle and proliferation of endothelial cells. The goal of this project is to elucidate the genes involved in vascular remodeling following pulmonary hypertension. Total RNA was isolated from lungs of normoxic and hypoxic treated animals.
2007-12-13 | E-GEOD-482 | biostudies-arrayexpress
Project description:Hypoxia can induce vasoconstriction followed by vascular remodeling including hypertrophy and hyperplasia of pulmonary vascular smooth muscle and proliferation of endothelial cells. The goal of this project is to elucidate the genes involved in vascular remodeling following pulmonary hypertension. Total RNA was isolated from lungs of normoxic and hypoxic treated animals. Keywords: other
2003-07-16 | GSE482 | GEO
Project description:PHD2/HIF-2 signaling regulates obliterative vascular remodeling and pulmonary arterial hypertension
| PRJNA304075 | ENA
Project description:Pulmonary hypertension is a frequent consequence of left heart disease and congestive heart failure (CHF) and causes extensive lung vascular remodelling which leads to right ventricular failure. Functional genomics underlying this structural remodelling are unknown but present potential targets for novel therapeutic strategies. We used microarrays to detail the gene expression underlying vascular remodeling in the pathogenesis of pulmonary hypertension and identified distinct classes of up-regulated genes during this process. Control rat lung samples were compared to samples of aortic banding rat lungs which exhibit pulmonary hypertension
2009-06-16 | E-GEOD-16624 | biostudies-arrayexpress
Project description:To determine roles by which infiltrating pulmonary intersitial macrophages regulate development and progression of pulmonary vascular remodeling and pulmonary hypertension.
2020-01-07 | GSE143142 | GEO
Project description:Pulmonary hypertension (PH), a common complication in dogs affected by degenerative mitral valve disease (DMVD), is a progressive disorder characterized by increased pulmonary arterial pressure (PAP) and pulmonary vascular remodeling. Early diagnosis of PH is crucial for effective management and improved clinical outcomes. This study aimed to identify potential serum biomarkers for diagnosing PH in dogs affected with DMVD using a phosphoproteomic approach.
2023-10-30 | PXD046218 | JPOST Repository
Project description:Pulmonary arterial hypertension (PAH) is a progressive pulmonary vascular disease that culminates in right heart failure. Vascular pathology in PH is characterized by pulmonary vasoconstriction and progressive vascular remodeling processes that affects all layers of the vascular wall (intima, media and adventitia).
2022-06-09 | GSE194080 | GEO
Project description:	Pulmonary hypertension (PH), a common complication in dogs affected by degenerative mitral valve disease (DMVD), is a progressive disorder characterized by increased pulmonary arterial pressure (PAP) and pulmonary vascular remodeling. Early diagnosis of PH is crucial for effective management and improved clinical outcomes. This study aimed to identify potential serum biomarkers for diagnosing PH in dogs affected with DMVD using a phosphoproteomic approach.
2024-04-10 | PXD050923 | JPOST Repository
Project description:Pulmonary veno-occlusive disease (PVOD) is a rare and severe form of pulmonary arterial hypertension, characterized by progressive obstruction of small pulmonary vessels and a lack of effective therapeutic options. Our previous research, utilizing a mitomycin C (MMC)-induced rat model, demonstrated that activation of the integrated stress response (ISR) via protein kinase R (PKR) is a critical driver of endothelial dysfunction and pulmonary vascular remodeling. However, it remains unclear whether PKR is the sole mediator of ISR activation and the pathogenesis of PVOD under the MMC treatment. In this study, we administered the same dose of MMC used in rats to control (Ctrl) and PKR knockout (KO) mice. Consistent with observations in rats, Ctrl mice exhibited ISR activation in the vascular endothelium and rapidly developed vascular remodeling in both arteries and veins following MMC treatment. In contrast, KO mice showed no evidence of ISR activation or vascular remodeling under same conditions. Proteomic analysis revealed that the PKR-ISR axis perturbs proteostasis in Ctrl mice but not in KO mice. These findings highlight the essential role of PKR-mediated ISR activation and the disruption of proteostasis in the pathogenesis of PVOD, placing PKR as a promising therapeutic target for this disease.
2025-08-11 | PXD066782 | Pride
Project description:Rationale: Schistosomiasis is one of the most common causes of pulmonary arterial hypertension worldwide, but the pathogenic mechanism by which the host inflammatory response contributes to vascular remodeling is unknown. We sought to identify signaling pathways that play protective or pathogenic roles in experimental Schistosoma-induced pulmonary vascular disease by whole-lung transcriptome analysis. Methods: Wildtype mice were experimentally exposed to S. mansoni ova by intraperitoneal sensitization followed by tail vein augmentation, and the phenotype assessed by right ventricular catheterization and tissue histology, RNA and protein analysis. Whole-lung transcriptome analysis by microarray and RNA sequencing was performed, the latter analyzed using 2 bioinformatic methods. Functional testing of the candidate IL-6 pathway was determined using IL6-knockout mice and the STAT3 inhibitor STI-201. Results: Wild-type mice exposed to S. mansoni had increased right ventricular systolic pressure and thickness of the pulmonary vascular media. Whole lung transcriptome analysis identified the IL6-STAT3-NFATc2 pathway as being upregulated, which was confirmed by PCR and immunostaining of lung tissue from S. mansoni-exposed mice and patients who died of the disease. Mice lacking IL6 or treated with STI-201 developed pulmonary hypertension associated with significant intima remodeling after exposure to S. mansoni. Conclusions: Whole lung transcriptome analysis identified upregulation of the IL6-STAT3-NFATc2 pathway, and IL6 signaling was found to be protective against Schistosoma-induced intimal remodeling. Affy Mouse ST1.0 chip used. Whole lung transcriptome of 3 mice with experimental Schistosoma-induced pulmonary hypertension, compared to 3 control mice. All mice on a C57Bl6/J background.
2013-07-16 | E-GEOD-48936 | biostudies-arrayexpress