Project description:Hypoxia is used as a model for pulmonary arterial hypertension. MiR-145 is upregulated in pulmonary arterial hypertension in humans and female mice. It has been observed that miR-145 knock out mice have reduced vascular remodelling in response to hypoxia. Therefore, knock down of miR-145 could be used as a therapy for pulmonary arterial hypertension in humans. This microarray has helped us to elucidate some of the pathways in the miR-145 knock out mice that may protect against vascular remodelling. Wild type (WT) mice and homozygous miR-145 -/- female mice (strain C57BL6J/129SVEV) at 8 weeks old were exposed to chronic hypoxia for 2 weeks or maintained in normoxic conditions and pulmonary arteries were dissected at 10 weeks of age. This study contained 4 groups, WT hypoxic, WT normoxic, miR-145 -/-, hypoxic miR-145 -/- normoxic each containing 6 animals. All adjacent comparisons were made to ananlyse the data (a 2 by 2 design).
Project description:Whole exome sequencing of 41 melanomas and normal DNA from Braf mutant mice: 15 tumours from UV exposed mice, 15 tumours from non-exposed mice and 11 from UV exposed, sunscreen-protected mice.
Project description:Expression data from mice exposed to intermittent hypoxia and mice reared for 12 months. We used microarrays to analyze the transcriptome of hippocampus from mice exposed to intermittent hypoxia or aged mice.
Project description:ApoE knockout mice were exposed to intermittent hypoxia and hypercapnia (treatment) or room air (controls). Perturbations in the gut microbiome were profiled longitudinally using LC-MS/MS to study the impact of treatment on the gut metabolome over the course of the day. Samples were collected after 6 days of exposure to conditions. Samples were collected every 4 hours for 24hrs (6 timepoints) to examine circadian rhythm dynamics.
Project description:ApoE knockout mice were either exposed to hypoxia, or hypercapnia, or both or kept in room air (controls) and fecal samples were collected longitudinally. Impact of treatments were studied using non-targeted LC-MS/MS data
Project description:Pulmonary arterial hypertension (PAH) is a chronic progressive disease with significant morbidity and mortality. The disease is characterized by vascular remodeling that includes increased muscularization of distal blood vessels and vessel stiffening associated with changes in extracellular matrix deposition. In humans, chronic hypoxia causes PAH, and hypoxia-induced rodent models of PAH have been used for years to study the disease. With the development of single-cell RNA sequencing technology, it is now possible to examine hypoxia-dependent transcriptional changes in vivo at a cell-specific level. In this study, we used single-cell RNA sequencing to compare lungs from wild-type mice exposed to hypoxia for 28 days to normoxia-treated control mice. We additionally examined mice deficient for Notch3, a smooth muscle-enriched gene linked to PAH. Data analysis revealed that hypoxia promoted cell number changes in immune and endothelial cell types in the lung, activated the innate immunity pathway, and resulted in specific changes in gene expression in vascular cells. Surprisingly, we found limited differences in lungs from mice deficient for Notch3 compared to wild-type controls. These findings provide novel insight into the effects of chronic hypoxia exposure on gene expression and cell phenotypes in vivo and identify unique changes to cells of the vasculature.
Project description:Mountain dwellers show a lower prevalence of diabetes, which among countless other factors could be due to lower partial oxygen pressure at high altitude. The present study was to investigate in an experimental setting, if and how reduced oxygen availability affects blood glucose. For hypothesis building, tissue samples were collected from obese mice on high fat diet, which were maintained under normal air (control) or exposed to normobaric hypoxia for three months. Tissue samples were collected and subjected to RNA sequencing and bioinformatics analysis. In a subsequent series of experiments, hypoxia-induced effects on fuel metabolism as well as the mechanism mediating such effects were studied. As compared to controls, hypoxia-treated mice showed reduced blood glucose in association with improved insulin sensitivity, which was the direct consequence of an erythropoietin-mediated increase in the hematocrit.
Project description:We exposed p14 mice to 56 day of forced intermittent hypoxia as a proxy stimlulus for pediatric OSA. After this exposure, we performed sn-RNA seq of the hippocampus of both normoxic controls and IH exposed mice to study potentially DEGs.
Project description:To explore the role played by senescent cells in mice models of pulmonary hypertension we exposed young C57BL6/j mice to 2 days hypoxia or normoxia and treated with senolytic drug ABT-263 (50mg/kg/day) or its vehicule. We then performed lung gene expression profiling analysis using data obtained from RNA-seq of 4 groups of mice (Normoxia+Vehicule; Normoxia+ABT-263; Hypoxia+Vehicule; Hypoxia+ABT-263)