Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-48936
PROVIDER: PRJNA213046 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Murine Schistosoma-Induced Pulmonary Hypertension: Microarray Data
| PRJNA212332 | ENA
Project description:Whole lung RNA-seq of 8 mice with experimental Schistosoma-induced pulmonary hypertension, compared to 8 control mice. All mice on a C57Bl6/J background. 3 schisto-PH and 3 control mice (#s 1-3 in each group) were also processed by Affy microarray and separately submitted. 3 of the mice in each group (labeled 1D11) were also treated with the pan-TGF-beta neutralizing antibody 1D11. Illumina HiSeq 2000 used. Data published in: Protective Role of IL6 in Vascular Remodeling in Schistosoma-Pulmonary Hypertension. Graham BB, Chabon J, Kumar R, Kolosionek E, Gebreab L, Debella E, Edwards M, Diener K, Shade T, Bifeng G, Bandeira A, Butrous G, Jones K, Geraci M, Tuder RM. Am J Respir Cell Mol Biol. 2013 Jul 1. [Epub ahead of print] PMID: 23815102 Whole lung transcriptome of 8 mice with experimental Schistosoma-induced pulmonary hypertension, compared to 8 control mice. All mice on a C57Bl6/J background.
2013-07-23 | E-GEOD-49114 | biostudies-arrayexpress
Project description:Schistosoma-pulmonary hypertension sorted macrophage gene expression
| PRJNA330737 | ENA
Project description:Whole lung RNA-seq of 8 mice with experimental Schistosoma-induced pulmonary hypertension, compared to 8 control mice. All mice on a C57Bl6/J background. 3 schisto-PH and 3 control mice (#s 1-3 in each group) were also processed by Affy microarray and separately submitted. 3 of the mice in each group (labeled 1D11) were also treated with the pan-TGF-beta neutralizing antibody 1D11. Illumina HiSeq 2000 used. Data published in: Protective Role of IL6 in Vascular Remodeling in Schistosoma-Pulmonary Hypertension. Graham BB, Chabon J, Kumar R, Kolosionek E, Gebreab L, Debella E, Edwards M, Diener K, Shade T, Bifeng G, Bandeira A, Butrous G, Jones K, Geraci M, Tuder RM. Am J Respir Cell Mol Biol. 2013 Jul 1. [Epub ahead of print] PMID: 23815102
2013-07-23 | GSE49114 | GEO
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
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. Data published in: Protective Role of IL6 in Vascular Remodeling in Schistosoma-Pulmonary Hypertension. Graham BB, Chabon J, Kumar R, Kolosionek E, Gebreab L, Debella E, Edwards M, Diener K, Shade T, Bifeng G, Bandeira A, Butrous G, Jones K, Geraci M, Tuder RM. Am J Respir Cell Mol Biol. 2013 Jul 1. [Epub ahead of print] PMID: 23815102
2013-07-16 | GSE48936 | GEO
Project description:Physiological shear stress, produced by blood flow, homeostatically regulates the phenotype of pulmonary endothelial cells exerting anti-inflammatory and anti-thrombotic actions and maintaining normal barrier function. In the pulmonary circulation hypoxia, due to high altitude or diseases such as COPD, causes vasoconstriction, increased vascular resistance and pulmonary hypertension. Hypoxia-induced changes in endothelial function play a central role in the development of this pulmonary hypertension. However, the direct interactive effects of hypoxia and shear stress on the pulmonary endothelial phenotype have not been extensively studied. We cultured human pulmonary microvascular endothelial cells (HPMEC) in normoxia or hypoxia while subjected to physiological shear stress or in static conditions. Unbiased proteomics was used to identify hypoxia-induced changes in protein expression. Using publicly available single cell RNA-seq datasets, differences in gene expression between the alveolar endothelial cells from COPD and healthy lungs were identified. 60 proteins were identified in HPMEC lysates whose expression changed in response to hypoxia in sheared but not in static conditions. mRNA for five of these (ERG, MCRIP1, EIF4A2, HSP90AA1 and DNAJA1) showed similar changes in the endothelial cells of COPD compared to healthy lungs. These data show that the proteomic responses of the pulmonary microvascular endothelium to hypoxia are significantly altered by shear stress and suggest that these differences are important in the development of hypoxic pulmonary vascular disease.
2023-02-17 | PXD036260 | Pride
Project description:Gene expression profile of lung with experimental Schistosoma-induced pulmonary hypertension in mouse
2015-10-12 | E-GEOD-48936 | ExpressionAtlas
Project description:Protective Role of IL6 in Vascular Remodeling in Schistosoma-Pulmonary Hypertension
| PRJNA213044 | ENA