Similar Datasets
Project description:Obstructive sleep apnea (OSA) results from episodes of airway collapse and intermittent hypoxia (IH) and is associated with a host of health complications. Although the lung is the first organ to sense changes in oxygen levels, little is known about the consequences of IH to the lung hypoxia-inducible factor-responsive pathways. We hypothesized that exposure to IH would lead to cell-specific up- and downregulation of diverse expression pathways. We identified changes in circadian and immune pathways in lungs from mice exposed to IH. Among all cell types, endothelial cells showed the most prominent transcriptional changes. Upregulated genes in myofibroblast cells were enriched for genes associated with pulmonary hypertension and included targets of several drugs currently used to treat chronic pulmonary diseases. A better understanding of the pathophysiologic mechanisms underlying diseases associated with OSA could improve our therapeutic approaches, directing therapies to the most relevant cells and molecular pathways.
| S-EPMC7909952 | biostudies-literature
Project description:Obstructive sleep apnea (OSA) results from episodes of airway collapse and intermittent hypoxia (IH) and is associated with a host of health complications. Although the lung is the first organ to sense changes in oxygen levels, little is known about the consequences of IH to the lung hypoxia-inducible factor- (HIF)-responsive pathways. We hypothesized that exposure to IH would lead to cell-specific up and downregulation of diverse expression pathways. We identified changes in circadian and immune pathways in lungs from mice exposed to IH. Among all cell types, endothelial cells showed the most prominent transcriptional changes. Upregulated genes in myofibroblast cells were enriched for genes associated with pulmonary hypertension and included targets of several drugs currently used to treat chronic pulmonary diseases. A better understanding of the pathophysiologic mechanisms underlying diseases associated with OSA could improve our therapeutic approaches, directing therapies to the most relevant cells and molecular pathways.
2021-02-18 | GSE145434 | GEO
Project description:Obstructive sleep apnea (OSA) results from episodes of airway collapse and intermittent hypoxia (IH) and is associated with a host of health complications. Although the lung is the first organ to sense changes in oxygen levels, little is known about the consequences of IH to the lung hypoxia-inducible factor- (HIF)-responsive pathways. We hypothesized that exposure to IH would lead to cell-specific up and downregulation of diverse expression pathways. We identified changes in circadian and immune pathways in lungs from mice exposed to IH. Among all cell types, endothelial cells showed the most prominent transcriptional changes. Upregulated genes in myofibroblast cells were enriched for genes associated with pulmonary hypertension and included targets of several drugs currently used to treat chronic pulmonary diseases. A better understanding of the pathophysiologic mechanisms underlying diseases associated with OSA could improve our therapeutic approaches, directing therapies to the most relevant cells and molecular pathways.
2021-02-18 | GSE145435 | GEO
Project description:Short-term exposure to intermittent hypoxia leads to changes in gene expression seen in chronic pulmonary disease
| PRJNA607212 | ENA
Project description:Short-term exposure to intermittent hypoxia leads to changes in gene expression seen in chronic pulmonary disease [bulk RNA]
| PRJNA607214 | ENA
Project description:Short-term exposure to intermittent hypoxia leads to changes in gene expression seen in chronic pulmonary disease [single-cell RNA]
| PRJNA607217 | ENA
Project description:ObjectiveTo investigate the effect of short-term intermittent hypoxia (IH) on the structure and function of mouse myocardium.MethodsThirty male C57BL6/J mice were randomly assigned to two groups, a control (Con) group and an IH group exposed to hypoxic treatment at atmospheric pressure. The IH group received 10% oxygen pretreatment for 8 hours per day on 14 consecutive days, while the Con group was exposed to normoxia environment and all the other treatment the group received were identical to those given to the IH group, The body mass of the mice was monitored daily during the treatment. The exercise tolerance and the cardiac function of isolated heart were assessed at the end of IH exposure. Additionally, analysis was conducted regarding myocardial enzymology, histology, and other indicators relevant to oxidative stress, including protein carbonylation and lipid peroxidation.ResultsThere was no significant difference in the exercise tolerance between the two groups. Nevertheless, IH mice showed enhanced cardiac function during isolated heart perfusion ( P<0.05). As compared to the control group, prominent alterations of myocardial structure were detected by transmission electron microscopy of the IH heart, accompanied by elevated creatine kinase-MB levels ( P<0.05). The levels of myocardial reactive oxygen species, protein carbonylation and lipid peroxidation were all significantly upregulated in the IH group as compared to the control group ( P<0.05).ConclusionIH exposure induced myocardial oxidative stress damage and myofibrillar structural alteration in mice, but did not impair the exercise tolerance of the mice or the contractile function of the isolated heart.
| S-EPMC10408848 | biostudies-literature
Project description:Prediction of adverse health effects at altitude or during air travel is relevant, particularly in pre-existing cardiopulmonary disease such as pulmonary arterial or chronic thromboembolic pulmonary hypertension (PAH/CTEPH, PH). A total of 21 stable PH-patients (64 ± 15 y, 10 female, 12/9 PAH/CTEPH) were examined by pulse oximetry, arterial blood gas analysis and echocardiography during exposure to normobaric hypoxia (NH) (FiO2 15% ≈ 2500 m simulated altitude, data partly published) at low altitude and, on a separate day, at hypobaric hypoxia (HH, 2500 m) within 20−30 min after arrival. We compared changes in blood oxygenation and estimated pulmonary artery pressure in lowlanders with PH during high altitude simulation testing (HAST, NH) with changes in response to HH. During NH, 4/21 desaturated to SpO2 < 85% corresponding to a positive HAST according to BTS-recommendations and 12 qualified for oxygen at altitude according to low SpO2 < 92% at baseline. At HH, 3/21 received oxygen due to safety criteria (SpO2 < 80% for >30 min), of which two were HAST-negative. During HH vs. NH, patients had a (mean ± SE) significantly lower PaCO2 4.4 ± 0.1 vs. 4.9 ± 0.1 kPa, mean difference (95% CI) −0.5 kPa (−0.7 to −0.3), PaO2 6.7 ± 0.2 vs. 8.1 ± 0.2 kPa, −1.3 kPa (−1.9 to −0.8) and higher tricuspid regurgitation pressure gradient 55 ± 4 vs. 45 ± 4 mmHg, 10 mmHg (3 to 17), all p < 0.05. No serious adverse events occurred. In patients with PH, short-term exposure to altitude of 2500 m induced more pronounced hypoxemia, hypocapnia and pulmonary hemodynamic changes compared to NH during HAST despite similar exposure times and PiO2. Therefore, the use of HAST to predict physiological changes at altitude remains questionable. (ClinicalTrials.gov: NCT03592927 and NCT03637153).
| S-EPMC9147287 | biostudies-literature
Project description:Atherosclerosis is the pathological basis of cardiovascular disease. Obstructive sleep apnea aggravates atherosclerosis, and chronic intermittent hypoxia (CIH) as a prominent feature of obstructive sleep apnea plays an important role during the process of atherosclerosis. The mechanisms of CIH in the development of atherosclerosis remain unclear. The microarray was used to investigate differentially expressed mRNAs and long noncoding RNAs (lncRNAs) in aorta from five groups of ApoE-/- mice fed with a high-fat diet and exposed to various conditions: normoxia for 8 weeks, CIH for 8 weeks, normoxia for 12 weeks, CIH for 12 weeks, or CIH for 8 weeks followed by normoxia for 4 weeks.
2020-02-14 | GSE145221 | GEO
Project description:Obstructive sleep apnea, a condition leading to chronic intermittent hypoxia (CIH), is associated with hyperlipidemia, atherosclerosis, and a high cardiovascular risk. A causal link between obstructive sleep apnea and atherosclerosis has not been established.The objective of the present study was to examine whether CIH may induce atherosclerosis in C57BL/6J mice.Forty male C57BL/6J mice, 8 weeks of age, were fed either a high-cholesterol diet or a regular chow diet and subjected either to CIH or intermittent air (control conditions) for 12 weeks.Nine of 10 mice simultaneously exposed to CIH and high-cholesterol diet developed atherosclerotic lesions in the aortic origin and descending aorta. In contrast, atherosclerosis was not observed in mice exposed to intermittent air and a high-cholesterol diet or in mice exposed to CIH and a regular diet. A high-cholesterol diet resulted in significant increases in serum total and low-density lipoprotein cholesterol levels and a decrease in high-density lipoprotein cholesterol. Compared with mice exposed to intermittent air and a high-cholesterol diet, combined exposure to CIH and a high-cholesterol diet resulted in marked progression of dyslipidemia with further increases in serum total cholesterol and low-density lipoprotein cholesterol (124 +/- 4 vs. 106 +/- 6 mg/dl; p < 0.05), a twofold increase in serum lipid peroxidation, and up-regulation of an important hepatic enzyme of lipoprotein secretion, stearoyl-coenzyme A desaturase-1.CIH causes atherosclerosis in the presence of diet-induced dyslipidemia.
| S-EPMC2176090 | biostudies-other