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PROVIDER: PRJNA828538 | ENA |
REPOSITORIES: ENA
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Project description:Experiments in rodents have shown that kidney ischemia/reperfusion injury (IRI) facilitates lung injury and inflammation. To identify potential ischemia-specific lung molecular pathways involved, we conducted global gene expression profiling of lung 6 or 36 hours following 1) bilateral kidney IRI, 2) bilateral nephrectomy (BNx), and 3) sham laparotomy in C57BL/6J mice. Total RNA from whole lung was isolated and hybridized to 430MOEA (22,626 genes) GeneChips (n=3/group). Experiment Overall Design: All procedures were approved by the Johns Hopkins Animal Care and Use Committee, and were consistent with the National Institutes of Health (NIH) Guide for the Care and Use of Laboratory Animals. Male 6-8 week-old mice (C57BL6/J), weighing approximately 25-30 grams were obtained from Jackson Laboratory (Bar Harbor, ME) and housed under pathogen-free conditions according to NIH guidelines at least five days prior to operative procedures. Experiment Overall Design: Animals were placed on a heating blanket and underwent midline laparotomy with isolation of bilateral renal pedicles. For mice assigned to experimental ischemia-reperfusion injury (IRI), a non-traumatic microvascular clamp was applied across both renal pedicles for 60 minutes. After the allotted ischemia time, the clamps were gently removed, the animals administered 1 ml of sterile saline intraperitoneally, and the incision closed in two layers with 4-0 silk suture. The animals were then allowed to recover with free access to food and water. Sham animals underwent the identical procedure without placement of the vascular clamps. The mice assigned to bilateral nephrectomy (BNx) underwent similar procedures except both renal pedicles were ligated with 5-0 silk suture and the kidneys removed. At 6 or 36 hours following the experimental procedure, the mice were euthanized by exsanguination under pentobarbital anesthesia and lung tissues collected for analysis.
2008-06-15 | E-GEOD-6730 | biostudies-arrayexpress
Project description:To examine the age-related vulnerability to lung ischemia reperfusion injury, pulmonary gene expression profiles after lung ischemia reperfusion were compared between young and old mice.
2024-04-06 | GSE211951 | GEO
Project description:Intestinal ischemia-reperfusion (IR) injury is initiated when natural IgM antibodies recognize neo-epitopes that are revealed on ischemic cells. The target molecules and mechanisms whereby these neo-epitopes become accessible to recognition are not well understood. Proposing that isolated intestinal epithelial cells (IEC) may carry IR-related neo-epitopes, we used in vitro IEC binding assays to screen hybridomas created from B cells of unmanipulated wild type C57BL/6 mice. We identified a novel IgM monoclonal antibody (mAb B4) that reacted with the surface of IEC by flow cytometric analysis and was alone capable of causing complement activation, neutrophil recruitment and intestinal injury in otherwise IR-resistant Rag1-/- mice. Monoclonal Ab B4 was found to specifically recognize mouse annexin IV. Pre-injection of recombinant annexin IV blocked IR injury in wild type C57BL/6 mice, demonstrating the requirement for recognition of this protein in order to develop IR injury in the context of a complex natural antibody repertoire. Humans were also found to exhibit IgM natural antibodies that recognize annexin IV. These data in toto identify annexin IV as a key ischemia-related target antigen that is recognized by natural Abs in a pathologic process required in vivo to develop intestinal IR injury. Keywords: Natural antibodies, Annexin, Ischemia Reperfusion, Inflammation, Complement In the study presented here, a total of 4 custom spotted antigen slides were hybridized with known antibodies.
2010-05-05 | E-GEOD-14862 | biostudies-arrayexpress
Project description:Heart disease remains the leading cause of death globally. Although reperfusion following myocardial ischemia can prevent death by restoring nutrient flow, ischemia/reperfusion injury can cause significant heart damage. The mechanisms that drive ischemia/reperfusion injury are not well understood; currently, few methods can predict the state of the cardiac muscle cell and its metabolic conditions during ischemia. Here, we explored the energetic sustainability of cardiomyocytes, using a model for cellular metabolism to predict the levels of ATP following hypoxia. We modeled glycolytic metabolism with a system of coupled ordinary differential equations describing the individual metabolic reactions within the cardiomyocyte over time. Reduced oxygen levels and ATP consumption rates were simulated to characterize metabolite responses to ischemia. By tracking biochemical species within the cell, our model enables prediction of the cell’s condition up to the moment of reperfusion. The simulations revealed a distinct transition between energetically sustainable and unsustainable ATP concentrations for various energetic demands. Our model illustrates how even low oxygen concentrations allow the cell to perform essential functions. We found that the oxygen level required for a sustainable level of ATP increases roughly linearly with the ATP consumption rate. An extracellular O2 concentration of ~0.007 mM could supply basic energy needs in non-beating cardiomyocytes, suggesting that increased collateral circulation may provide an important source of oxygen to sustain the cardiomyocyte during extended ischemia. Our model provides a time-dependent framework for studying various intervention strategies to change the outcome of reperfusion.
2020-08-25 | BIOMD0000000961 | BioModels
Project description:Lung tissue samples from mice in lung ischemia-reperfusion injury (LIRI) group (ischemia for 1 hour and reperfusion for 6 hours) and sham groups were used for quantitative proteomics analysis.
2023-08-28 | PXD044899 | iProX
Project description:Lung ischemia-reperfusion (I/R) injury remains one of the common complications after various cardiopulmonary surgeries. I-R injury represents one potentially maladaptive response of the innate immune system which is featured by an exacerbated sterile inflammatory response triggered by tissue damage. Thus, understanding the key components and processes involved in sterile inflammation during lung I-R injury is critical to alter care and extend survival for patients with acute lung injury. We constructed a minipig surgical model of transient unilateral left pulmonary artery occlusion without bronchial involvement to create ventilated lung I-R injury. Lung tissues from minipig with sham operation (one sample), left side lung tissues (the operated side)(one sample) and right side lung tissues (the non-operated side)(one sample) from minipig with lung ischemia-reperfusion were submitted for gene expression array analysis.
2015-12-07 | E-GEOD-75560 | biostudies-arrayexpress
Project description:Purpose：Detection of differentially expressed lncRNA in the infarct zone and the control group in myocardial ischemia-reperfusion injury model tissue. Method: Use 8 weeks of C57BL/6 mice to establish a myocardial ischemia-reperfusion injury model, 45 minutes of ischemia, and 24 hours after reperfusion, the mice were sacrificed to obtain materials. Result: The expression of lncRNAs in the infarct area of myocardial ischemia-reperfusion injury model mice was detected, and it was found that a total of 43 lncRNAs related to myocardial ischemia-reperfusion injury changed in expression, of which 17 were up-regulated (fold change >1.5). 26 expressions are down-regulated (fold change <0.8)
2020-11-11 | GSE161151 | GEO
Project description:Ischemia reperfusion induced injury contributes to poor lung transplant outcomes.Microarrays were used to study the biological response of human lungs to the ischemia reperfusion process. Samples were collected from lung transplant cases at Toronto General Hospital. Lungs were donation after brain death (DBD)
2023-09-18 | GSE127242 | GEO
Project description:Ischemia reperfusion induced injury contributes to poor lung transplant outcomes. We used microarrays to study the biological response of human lungs to the ischemia reperfusion process. Samples were collected from lung transplant cases at Toronto General Hospital. Lungs were donation after brain death (DBD)
2020-06-22 | GSE127003 | GEO