Transcriptome Analysis Reveals Gene Expression Changes in a mouse Model of Hyperoxia-induced acute lung injury
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE237260 | GEO | 2024/04/05
REPOSITORIES: GEO
Similar Datasets
Project description:<p>Acute Respiratory Distress Syndrome (ARDS)/ Acute Lung Injury (ALI) is a syndrome defined by the presence of acute hypoxemic respiratory failure, bilateral pulmonary infiltrates on chest radiograph, a known clinical risk factor (e.g. sepsis, pneumonia, trauma, gastric fluid aspiration, pancreatitis, massive transfusion), and the absence of physiologic or clinical evidence of congestive heart failure.</p> <p>The Identification of SNPs Predisposing to Altered ALI Risk (iSPAAR) study is a multi-institutional cooperative study, funded through the NHLBI Recovery Act, that assembled samples and phenotype information from existing cohorts.</p> <p>The consortium included samples from patients with ARDS from the NIH NHLBI ARDS Clinical Trials Network (ARDSNet). Samples were obtained from 3 interventional treatment trials in patients with ARDS, including the Fluid and Catheter Treatment Trial (FACTT), the Albuterol to Treat Acute Lung Injury (ALTA) trial, and the Omega-3 Fatty Acid/Antioxidant Supplementation for ALI trial (Omega).</p> <p>In addition to ARDSnet samples, samples from the other cohorts included cases of established ARDS but also controls: critically ill patients who were at-risk for ARDS but who did not develop ARDS during their hospital course. These cohorts included the Molecular Epidemiology of Acute Respiratory Distress (MEA) Study enrolled at the Harvard University/Massachusetts General Hospital, the Systemic Inflammatory Immune Response Syndrome (SIRS) Patient Database and ICU Traumatic Injury cohorts from Harborview Medical Center, and cohorts collected from the ALI research programs at the University of Pennsylvania and the University of California, San Francisco.</p> <p><b>The Cohort is utilized in the following dbGaP sub-studies.</b> To view genotypes, other molecular data, and derived variables collected in these sub-studies, please click on the following sub-studies below or in the "Sub-studies" box located on the right hand side of this top-level study page <a href="study.cgi?study_id=phs000631">phs000631</a> ARDSnet iSPAAR Consortium. <ul> <li><a href="study.cgi?study_id=phs000334">phs000334</a> ESP_LungGO_ALI </li> <li><a href="study.cgi?study_id=phs000686">phs000686</a> ALI_GeneticRisk </li> </ul> </p>
| phs000631 | dbGaP
Project description:The acute respiratory distress syndrome (ARDS) is a common complications of severe COVID-19 and contributes to patient morbidity and mortality. ARDS is a heterogeneous syndrome caused by various insults, and results in acute hypoxemic respiratory failure. Patients with ARDS from COVID-19 may represent a subgroup of ARDS patients with distinct molecular profiles that drive disease outcomes. Here, we hypothesized that longitudinal transcriptomic analysis may identify distinct dynamic pathobiological pathways during COVID-19 ARDS. We identified a patient cohort from an existing ICU biorepository and established three groups for comparison: 1) patients with COVID-19 ARDS that survived hospitalization (COVID survivors, n = 4), 2) patients with COVID-19 ARDS that did not survive hospitalization (COVID non-survivors, n = 5), and 3) patients with ARDS from other causes as a control group (ARDS controls, n = 4). RNA was extracted from peripheral blood mononuclear cells (PBMCs) at 4 time points (Days 1, 3, 7, and 10 following ICU admission) and prepared for RNA sequencing with rRNA depletion and library generation for Illumina. An Illumina NovaSeq X Plus instrument was used to generate 150 base pair paired-end reads, which were aligned to the hg GRCh38.96 reference genome using HiSAT2. Differential expression analysis was performed with DESeq2.
2024-07-29 | GSE273149 | GEO
Project description:The causative organism, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), exhibits a wide spectrum of clinical manifestations in disease-ridden patients. Differences in the severity of COVID-19 ranges from asymptomatic infections and mild cases to the severe form, leading to acute respiratory distress syndrome (ARDS) and multiorgan failure with poor survival. MiRNAs can regulate various cellular processes, including proliferation, apoptosis, and differentiation, by binding to the 3′UTR of target mRNAs inducing their degradation, thus serving a fundamental role in post-transcriptional repression. Alterations of miRNA levels in the blood have been described in multiple inflammatory and infectious diseases, including SARS-related coronaviruses. We used microarrays to delineate the miRNAs and snoRNAs signature in the peripheral blood of severe COVID-19 cases (n=9), as compared to mild (n=10) and asymptomatic (n=10) patients, and identified differentially expressed transcripts in severe versus asymptomatic, and others in severe versus mild COVID-19 cases. A cohort of 29 male age-matched patients were selected. All patients were previously diagnosed with COVID-19 using TaqPath COVID-19 Combo Kit (Thermo Fisher Scientific, Waltham, Massachusetts), or Cobas SARS-CoV-2 Test (Roche Diagnostics, Rotkreuz, Switzerland), with a CT value < 30. Additional criterion for selection was age between 35 and 75 years. Participants were grouped into severe, mild and asymptomatic. Classifying severe cases was based on requirement of high-flow oxygen support and ICU admission (n=9). Whereas mild patients were identified based on symptoms and positive radiographic findings with pulmonary involvement (n=10). Patients with no clinical presentation were labelled as asymptomatic cases (n=10).
2022-03-01 | E-MTAB-10970 | biostudies-arrayexpress
Project description:Acute Respiratory Distress Syndrome (ARDS) is a very common clinical entity and a major cause of morbidity and mortality in the critical care setting. Historically, ARDS has been associated with mortality ranging from 40% to 60% . In the US alone,200,000 new cases of ARDS occur every year. ARDS can be associated with different clinical disorders affecting the lungs. A novel ex-vivo swine model developed by our group permits measurements of lung pathophysiology and simultaneous collection of lung and liver tissue for histologic and molecular comparisons during the early phase of the response to endotoxemia. In this preparation, endotoxemia causes a liver-dependent inflammatory response and severe lung injury and dysfunction. We chose swine, as an experimental animal because, like humans, they are especially sensitive to endotoxin and the pathophysiology of the response appears to be similar to that in humans. Gene expression was evaluated in swine liver before and after endotoxin treatment.
2013-01-10 | E-MTAB-1436 | biostudies-arrayexpress
Project description:Acute respiratory distress syndrome (ARDS) is a respiratory failure in critically ill patients, and the molecular mechanisms underlying its pathogenesis and severity are poorly understood. We evaluated mRNA and miRNA in patients with ARDS and elucidated the pathogenesis of ARDS, following mRNA and miRNA integration analysis. Thirty-four ARDS patients were compared with 15 healthy donors. 1233 mRNAs and 6 miRNAs were upregulated and 1580 mRNAs and 13 miRNAs were downregulated in ARDS patients compared healthy donors. In both mRNA and miRNA-targeted mRNA, the canonical pathway analysis showed that PD-1 and PD-L1 cancer immunotherapy pathway was most activated and Th2 pathway was most suppressed. miR-149-3p and several miRNAs were identified as upstream regulators. Integrated analysis of mRNAs and miRNAs showed that T cells were dysfunctional in ARDS patients.
2024-03-15 | GSE243066 | GEO
Project description:Acute respiratory distress syndrome (ARDS) is a respiratory failure in critically ill patients, and the molecular mechanisms underlying its pathogenesis and severity are poorly understood. We evaluated mRNA and miRNA in patients with ARDS and elucidated the pathogenesis of ARDS, following mRNA and miRNA integration analysis. Thirty-four ARDS patients were compared with 15 healthy donors. 1233 mRNAs and 6 miRNAs were upregulated and 1580 mRNAs and 13 miRNAs were downregulated in ARDS patients compared healthy donors. In both mRNA and miRNA-targeted mRNA, the canonical pathway analysis showed that PD-1 and PD-L1 cancer immunotherapy pathway was most activated and Th2 pathway was most suppressed. miR-149-3p and several miRNAs were identified as upstream regulators. Integrated analysis of mRNAs and miRNAs showed that T cells were dysfunctional in ARDS patients.
2024-03-15 | GSE243067 | GEO
Project description:Akap1 KO and Wt mice were exposed to normoxia or hyperoxia for 48h. Total RNA was extracted from lungs of Wt Normoxia (n=3), Wt hyperoxia (n=3), Akap1 KO (n=3) and Akap1 hyperoxia (n=3) mice. RNA-sequencing was carried out followed by differential expression of genes in the following groups. Wt Normoxia vs Wt Hyperoxia, Akap1 KO Normoxia versus Akap1 KO Hyperoxia, Wt Normoxia versus Akap1 KO Normoxia and Wt Hperoxia versus Akap1 Hyperoxia.
2022-10-26 | GSE173295 | GEO
Project description:Despite a significant progress in the treatment of Acute Respiratory Distress Syndrome (ARDS), our ability to identify early patients and predict outcome remains limited. In this study, we aimed to characterize small RNA content of plasma exosomes from ARDS patients in order to identify potential diagnostic biomarkers of the disease. For the first time, we profiled miRNA expression levels in plasma-derived exosomes from ARDS patients (n=8) compared to healthy subjects (n=10) by small RNA-seq. It allowed us to identify 12 exosomal miRNAs differentially expressed in ARDS context (padj<0.05).
2021-01-19 | E-MTAB-9991 | biostudies-arrayexpress
Project description:We aimed to identify endotypes of pediatric acute respiratory distress syndrome (ARDS) using whole blood transcriptomics collected within 24 hours of Berlin ARDS onset in intubated children from CHOP Affy microarray and cluster analysis
2020-04-02 | GSE147902 | GEO
Project description:Our previous data obtained by using immunohistochemistry showed, that Fgf10+/- (50% Fgf10 expression compared to WT) in hyperoxic condition at postnatal day 3 (P3) compared to WT has less vessel count in the lung and less muscularization of small capillaries in the lung. Furthermore, Fgf10+/- showed a drastic increase in mortality upon hyperoxic lung injury. Main question to be answer by this experiment is as followed: Does Fgf10+/- mice after hyperoxia from P0-P3 show different expression profiles at P3 compared to WT? To adress this question we harvest lungs at P3 from WT and Fgf10+/- after hyperoxia treatment from P0-P3. For this the mice were sacrificed by Ketamin/ Dormitor ip, lungs were perfused transcardiac with PBS and directly frozen in liquid nitrogen.
2019-05-01 | GSE113102 | GEO