Hypoxia exposure and methylation
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE162606 | GEO | 2020/12/04
REPOSITORIES: GEO
Similar Datasets
Project description:Understanding molecular mechanism associated with high altitude exposure during acclimatization/adaptation/maladaptation. Data reveals specific components of the complex molecular circuitry underlying high altitude pulmonary edema. Individualized outcome prediction were constructed through expression profiling of 39400 genes in sea level sojourners who were acclimatized to high altitude and grouped as controls (n=14), high altitude natives (n=14) and individuals who developed high altitude pulmonary edema within 48-72 hours after air induction to high altitude (n=17).
2013-12-18 | E-GEOD-52209 | biostudies-arrayexpress
Project description:Hypoxia exposure and methylation
| PRJNA682379 | ENA
Project description:Understanding molecular mechanism associated with high altitude exposure during acclimatization/adaptation/maladaptation. Data reveals specific components of the complex molecular circuitry underlying high altitude pulmonary edema.
2013-12-18 | GSE52209 | GEO
Project description:Acute mountain sickness (AMS), which may progress to life-threatening high altitude cerebral edema, is a major threat to millions of people who live in or travel to high altitude. Although studies have revealed the risk factors and pathophysiology theories of AMS, the molecular mechanisms of it do not comprehensively illustrate. Here, we used a system-level methodology, RNA sequencing, to explore the molecular mechanisms of AMS at genome-wide level in 10 individuals. After exposure to high altitude, a total of 1,164 and 1,322 differentially expressed transcripts were identified in AMS and non-AMS groups, respectively. Among them, only 328 common transcripts presented between the two groups. Immune and inflammatory responses were overrepresented in participants with AMS, but not in non-AMS individuals. Anti-inflammatory cytokine IL10 and inflammation cytokines IF17F and CCL8 exhibited significantly different genetic connectivity in AMS compared to that of non-AMS individuals based on network analysis. IL10 was down-regulated and both IF17F and CCL8 were un-regulated in AMS individuals. Moreover, the serum concentration of IL10 significantly decreased in AMS patients after exposure to high altitude (p = 0.001) in another population (n=22). There was a large negative correlation between the changes of IL10 concentration, r(22) = -0.52, p = 0.013, and Lake Louise Score. Taken together, our analysis provides unprecedented characterization of AMS transcriptome and identifies that genes involved in immune and inflammatory responses were disturbed in AMS individuals by high altitude exposure. The reduction of IL10 after exposure to high altitude was associated with AMS.
2017-03-27 | GSE75665 | GEO
Project description:Acute mountain sickness (AMS) is a common disabling condition in individuals experiencing high altitudes, which may progress to life-threatening high altitude cerebral edema. Today, no established biomarkers are available for prediction of AMS and Non-AMS individuals before exposure to high altitude.MicroRNAs emerge as promising sensitive and specific biomarkers for a variety of diseases. Thus, we sought to identify circulating microRNAs suitable for prediction the susceptible of AMS before exposure to high altitude. A total of 31 microRNAs were differentially expressed between AMS and Non-AMS groups, 15 up-regulated and 16 down-regulated. Up-regulation of miR-369-3p, miR-449b-3p, miR-136-3p, and miR-4791 in patients with AMS compared with Non-AMS individuals were quantitatively confirmed using qPCR (all, P < 0.001). A unique signature encompassing miR-369-3p, miR-449b-3p, and miR-136-3p discriminate AMS from Non-AMS (area under the curve 0.986, 95%CI 0.970-1.000, P < 0.001, LR+: 14.21, LR-: 0.08). This signature yielded a 92.68% sensitivity and a 93.48% specificity for AMS vs. Non-AMS.The study here, for the first time, describes a signature of three circulating microRNAs as a robust biomarker to differentiate AMS from Non-AMS individuals.
2017-06-10 | GSE90500 | GEO
Project description:Altitude acclimatization is the physiological process to restore oxygen delivery to the tissues and promote the oxygen application under high altitude hypoxia. High altitude illness could happen in individuals who did not get acclimatization. Unraveling the molecular underpinnings of altitude acclimatization would help people to understand the beneficial response of body to high altitude hypoxia and disturbed biological process in un-acclimatized individuals. Here, we measured physiological adjustments and circulating microRNAs (cmiRNAs) profiles of individuals exposed to high altitude to explore the altitude acclimatization in humans.
2017-02-09 | GSE89486 | GEO
Project description:Background: Arachidonic acid (AA) metabolism pathway is dominant in metabolic programming after hypoxia exposure, but its biological function is disputed and require in-depth studies. In this research, we aimed at integrating plasma metabolomics and transcriptomics approaches to systematically explore its roles in response to acute hypoxia based on model of acute high-altitude exposure. Methods: Blood samples were taken from 53 enrolled subjects before and after their exposure to high altitude. Ultra-performance liquid chromatography- quadrupole time-of-flight mass spectrometry and RNA sequencing were performed to acquire corresponding metabolomic and transcriptomic profiling along with hypoxia exposure, separately. Influential modules comprising essential metabolites and genes were identified by weighted gene co-expression network analysis (WGCNA) after integrating metabolic information with phenotypic and transcriptomic datasets, respectively. Results: Enrolled individuals showed significant alterations in heart rate, SpO2, hemoglobin and Lake Louise Score (LLS) in response to hypoxia. Metabolomics profiling demonstrated that AA metabolism pathway was remarkable in these metabolic alterations. Integrated analysis of metabolomic and transcriptomic data revealed that increasing AA metabolism pathway might count for gas transport incapacitation and disorders in hemoglobin metabolism under hypoxia stimuli. Moreover, identified in further analysis and another cohort, excessively elevated AA metabolism pathway was involved in poor response to hypoxia. Conclusion: Our study, for the first time, constructed the maps of AA metabolism pathway in response to hypoxia; and revealed the crosstalk between phenotypic variation to hypoxia and AA metabolism pathway. These findings will not only advanced pathophysiological mechanisms for acute hypoxic diseases, but provided new insights into critical roles of AA metabolism pathway in development and prevention of these diseases.
2018-03-09 | GSE103940 | GEO
Project description:High-altitude hypoxia exposure inhibits erythrophagocytosis by inducing macrophage ferroptosis in the spleen
| PRJNA1095918 | ENA
Project description:For individuals migrating to or residing permanently at high-altitude regions, environmental hypobaric hypoxia is a primary challenge which induces several physiological or pathological responses. It is well documented that human beings adapt to hypobaric hypoxia via some protective mechanisms, such as erythropoiesis and overproduction of hemoglobin, however little is known on the changes of plasma proteome profiles in accommodation to high-altitude hypobaric hypoxia. In the present study, we investigated differential plasma proteomes of high altitude natives and lowland normal controls by a TMT-based proteomic approach. A total of 818 proteins were identified, of which 137 were differentially altered. Bioinformatics (including GO, KEGG, protein-protein interactions, etc.) analysis revealed the dysregulated proteins were primarily involved in complement and coagulation cascades, anti-oxidative stress and glycolysis. Validations via magnetic Luminex® Assays and ELISA demonstrated that CCL18, C9, PF4, MPO and S100A9 notably up-regulated, and HRG and F11 down-regulated in high altitude natives compared with lowland controls, which were consistent with the proteomic results. Our findings highlight the roles of complement and coagulation cascades, anti-oxidative stress and glycolysis in acclimatization to hypobaric hypoxia and provide a foundation for developing potential diagnostic or/and therapeutic biomarkers for high altitude hypobaric hypoxia-induced diseases.
2019-03-27 | PXD012221 | Pride
Project description:Hypoxia is associated with increased erythropoietin (EPO) release to drive erythropoiesis. However, a prolonged sojourn at high altitude results in an increase in EPO levels followed by a decrease, although erythropoiesis remains elevated at a stable level. The role of hypoxia and related EPO adjustments are not fully understood and contributed to the formulation of the theory of neocytolysis. In this study, we aimed to exclusively evaluate the role of oxygen on erythropoiesis comparing in vitro erythroid differentiation performed at atmospheric oxygen, with a lower oxygen concentration (3% O2) and with cultures of erythroid precursors isolated from peripheral blood after a 19-day sojourn at high altitude (3450 m). Results highlight an accelerated erythroid maturation at low oxygen and more concave morphology of reticulocytes. No differences in deformability were observed in the formed reticulocytes in the tested conditions. Moreover, hematopoietic stem and progenitor cells isolated from blood affected by hypoxia at high altitude did not result in a different erythroid development, suggesting no retention of high altitude signature but rather an immediate adaptation to oxygen concentration. This adaptation was observed during in vitro erythropoiesis at 3% oxygen, displaying a significantly increased glycolytic metabolic profile. These hypoxia-induced effects on in vitro erythropoiesis fail to provide an intrinsic explanation to the concept of neocytolysis.
2022-04-06 | PXD031776 | Pride