Rat right heart pulmonary embolism microarray
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE6104 | GEO | 2008/07/01
SECONDARY ACCESSION(S): PRJNA97549
REPOSITORIES: GEO
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Project description:Time and dose related expression profiles of rat right heart tissue in microsphere bead model for Pulmonary embolism Experiment Overall Design: Rat right tissues of the Vehicle(no beads- control), low dose and high dose from rat bead model for Pulmonary Embolism were collected after 2, 6 and 18 hour time points. The extracted RNA was hybridized to Affymetrix Rat 230-2.0 microarrays to look for the dose and/or time related transcriptional changes associated with experimental Pulmonary Embolism.
2008-10-18 | E-GEOD-6104 | biostudies-arrayexpress
Project description:Rats were given pulmonary embolism by i.v. injection of 25 micron polystyrene microspheres or 0.01% Tween20 solution as vehicle control Embolism of microspheres is irreversible and causes dose dependent pulmonary hypertension Keywords: time course and dose response
2009-09-01 | GSE13535 | GEO
Project description:Pulmonary vascular occlusions due to thromboemboli can result in pulmonary hypertension and right heart damage. Treatments to clear the vascular obstructions such as i.v. heparain or thrombolytics can resolve the hypertension but right ventricular damage often occurs first. Methods of protecting the right ventricle from hypertensive damage during the course of acute treatment to clear the thromboemboli are needed. Monocyte- and neutrophil-mediated inflammation and fibrosis are associated with chronic right ventricular damage but the pathways involved are not understood. A comprehesive survey of gene expression during chronic pulmonary embolism verses control rats has been conducted in this study.
2009-09-01 | GSE11851 | GEO
Project description:Right ventricular failure was induced thourgh pulmonary banding in 11 pigs. Right ventricular failure was defined as a SRVP >50 mmHg during two hours. After right ventricular failure was induced, half the pigs were treatmed with a Glenn-shunt combined with pulmonary banding for one hour, and the other half served as control group with pulmonary banding only. The aim was to study the change in global gene expression during right ventricular failure due to pulmonary banding, and the effect of volume unloading during pulmonary banding. 11 pigs. Samples at the following time periods: 1) Baseline 2) Right ventricular failure 3) Treatment with modified Glenn-shunt/Control. After Right ventricular failure, pigs were divided into two groups a) Treatment with modified Glenn-shunt or b) Control group
2013-06-11 | E-GEOD-47814 | biostudies-arrayexpress
Project description:Right ventricular failure was induced thourgh pulmonary banding in 11 pigs. Right ventricular failure was defined as a SRVP >50 mmHg during two hours. After right ventricular failure was induced, half the pigs were treated with a Glenn-shunt combined with pulmonary banding for one hour, and the other half served as control group with pulmonary banding only. The aim was to study the change in global gene expression during right ventricular failure due to pulmonary banding, and the effect of volume unloading during pulmonary banding.
2013-06-11 | GSE47814 | GEO
Project description:Rat right heart pulmonary embolism microarray
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Project description:RNA was isolated from plasma of 20 healthy patients and 20 patients with acute pulmonary embolism. Dysregulated microRNA patterns were screened in these samples
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Project description:Gene expression in rat right ventricles during chronic pulmonary embolism
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Project description:Pulmonary embolism (PE) is a life-threatening disease. Our aim was to search for potential biomarkers using modern high-throughput metabolomics methods to improve diagnostic efficacy. The discovery cohort included 60 participants, including 30 PE patients and 30 healthy individuals. The validation cohort had 40 participants, including 20 PE patients and 20 healthy individuals. Gas chromatography-mass spectrometry (GC-MS) was combined with multivariate data analysis to determine serum metabolic profiles in patients with PE and healthy controls. The distribution of metabolic profiles in the two cohorts was assessed by unsupervised principal component analysis (PCA) and supervised partial least squares discriminant analysis (PLS-DA). Sixteen metabolites were selected from the ranked variable of predictive importance (VIP) scores and applied to the correlation analysis of PE-related clinical indicators. Four metabolites that were correlated with D-dimer levels were selected, including L-tryptophan, N-α-acetyl-L-lysine, dopamine, and N2-acetylornithine. Finally, the AUC values were calculated to be 0.958 (95% CI: 0.9122-1) for the combined biomarker panel including the 4 specific metabolites in the discovery cohort and 0.963 (95% CI: 0.9122-1) in the validation cohort. The results suggest that these four specific metabolites can be used as diagnostic biomarkers to improve diagnostic efficacy in pulmonary embolism.
2024-10-24 | PXD057168 |
Project description:Right ventricular (RV) failure is the major determinant of outcome in pulmonary hypertension (PH). Calves exposed to 2-wks environmental hypoxia develop severe PH and unlike rodents, chronic hypoxia-induced PH in this species can lead to right heart failure. We therefore sought to examine the molecular and structural changes in the RV in calves with hypoxia-induced PH, hypothesizing that we could identify mechanisms underlying compensated physiological function in the face of developing severe PH. Calves were exposed to 14d of hypobaric hypoxia (PB=430 mm Hg, equivalent to 4570m elevation, n=29) or ambient normoxia (1525m, n=25). Cardiopulmonary function was evaluated by right heart catheterization and pressure volume loops. Molecular and cellular determinants of RV remodeling were analyzed by cDNA microarrays, RealTime PCR, proteomics and immunochemistry. Hypoxic exposure induced robust PH, with increased RV contractile performance and preserved cardiac output, yet evidence of dysregulated RV-pulmonary artery mechanical coupling consistent with advanced PH. Analysis of gene expression revealed cellular processes associated with structural remodeling, cell signaling, and survival. We further identified specific clusters of gene expression associated with (i) hypertrophic gene expression and pro-survival mechanotransduction through YAP-TAZ signaling, (ii) ECM remodeling, (iii) inflammatory cell activation and (iv) angiogenesis. A potential transcriptomic signature of cardiac fibroblasts in RV remodeling was detected. Proteomic and immunohistochemical analysis confirmed RV myocyte hypertrophy, together with localization of ECM remodeling, inflammatory cell activation, and endothelial cell proliferation within the RV interstitium. In conclusion, hypoxia and hemodynamic load initiate coordinated processes of protective and compensatory RV remodeling to withstand the progression of PH.
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