Homo sapiens
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PROVIDER: PRJNA128245 | ENA |
REPOSITORIES: ENA
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Project description:Gene Expression of muscle tissue during microsurgical free tissue transfer was basicly studied in animal models. There was found activation of inflammatory and apoptotic cascades and of genes regulating intracellular metabolism. We used microarrays to detail the programme of gene expression in human muscle tissue which is activated during this process. Human muscle which was harvested during microsurgical free tissue transfer was used for RNA extraction and hybridization on Affymetrix microarrays. Muscle samples of the flap were taken during normoxia (I) after ischemia (II) and after reperfusion (III). Ischemia startet after dissecting the sustentative vessel. Reperfusion began after reanastomosing the vessel and restoring the blood supply.
2010-07-07 | E-GEOD-22761 | 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.
2024-09-02 | BIOMD0000000961 | BioModels
Project description:This is an ordinary differential equation model of the early inflammatory response during transplantion. Descriptions are included of the inflammatory events associated with the initial surgical procedure, the subsequent ischemia/reperfusion (I/R) events that cause tissue damage to the host as well as the donor graft, and the inflammatory effects of T cells.
2019-11-19 | MODEL1911190001 | BioModels
Project description:Hepatic ischemia reperfusion injury is a dynamic process consisting of two stages: ischemia and reperfusion, and triggers a cascade of physiological and biochemical events. Given the important role of microRNAs in regulating gene expression, we analyzed gene expression changes in mouse livers at sham control, ischemia stage, and reperfusion stage. We generated global expression profiles of microRNA and mRNA genes in mouse livers subjected to ischemia reperfusion injury at the three stages, respectively. Comparison analysis showed that reperfusion injury had a distinct expression profile whereas the ischemia sample and the sham control were clustered together. Consistently, there are 69 differentially expressed microRNAs between the reperfusion sample and the sham control whereas 28 differentially expressed microRNAs between the ischemia sample and the sham control. We further identified two modes of microRNA expression changes in ischemia reperfusion injury. Functional analysis of both the differentially expressed microRNAs in the two modes and their target mRNAs revealed that ischemia injury impaired mitochondria function, nutrient consumption, and metabolism process. In contrast, reperfusion injury led to severe tissue inflammation that is predominantly an innate-immune response in the ischemia reperfusion process. Our staged analysis of gene expression profiles provides new insights into regulatory mechanisms of microRNAs in mouse hepatic ischemia reperfusion injury.
2015-10-01 | GSE72314 | GEO
Project description:Early Gene Expression Profiles During Intraoperative Myocardial Ischemia-Reperfusion in Cardiac Surgery
| PRJNA99553 | ENA
Project description:Purpose: Acute kidney injury (AKI) is defined as a sudden event of kidney failure or kidney damage occurring within a short period. Ischemia-reperfusion injury (IRI) is a critical factor to induce severe AKI and end-stage kidney disease in the kidney. However, biological mechanisms of ischemia and reperfusion are not well elucidated due to its complex pathophysiological processes. We aim to investigate key biological pathways affected by ischemia and by reperfusion separately at the transcriptome level. Method: We analyzed steady-state gene expressions using RNA-seq transcriptome data for normal (pre-ischemia), ischemia and reperfusion conditions obtained from the human kidney tissue. A conventional differential expression analysis and self-organizing map (SOM) clustering analysis followed by pathway analysis were performed to identify the underlying biological mechanisms of ischemia and reperfusion. Results: Differential expression analysis showed that metabolism and gap junction-related pathways were dysregulated in ischemia, whereas hypertrophy and immune response-related pathways were dysregulated in reperfusion. In addition, SOM clustering analysis revealed that metabolism, apoptosis, and fibrosis-related pathways were significantly dysregulated by ischemia compared to pre-ischemia. On the other hand, cell growth, migration, and immune response-related pathways were highly dysregulated by reperfusion after ischemia. Pro-apoptotic genes and death receptors were down-regulated during ischemia, indicating a protective process against ischemic injury. Reperfusion induced alteration of genes associated with immune components such as B-cell, neutrophil, and interleukin-15. Additionally, genes related to cell growth and migration such as AKT, KRAS, and Rho signaling were down-regulated, which might imply injury responses during reperfusion. Semaphorin 4D and plexin B1 were also down-regulated. However, further investigations are needed to identify their roles. Conclusion: We showed that specific biological pathways were distinctively involved in ischemia and reperfusion during IRI, suggesting that condition-specific therapeutic strategies may be required to prevent severe kidney damage after IRI in clinical research.
2019-12-17 | GSE142077 | GEO
Project description:Disruption of peripheral circadian rhyme pathways dominantly leads to metabolic disorders. Studies on circadian rhythm proteins in the heart indicated a role for Clock or Per2 in cardiac metabolism. In fact, Per2-/- mice have larger infarct sizes with a deficient lactate production during myocardial ischemia. To test the hypothesis that cardiac Per2 represents an important regulator of cardiac metabolism during myocardial ischemia, we performed lactate measurements during reperfusion in Per1-/-, Per2-/- or wildtype mice followed by gene array studies using various ischemia-reperfusion protocols comparing wildtype and Per2-/- mice. Lactate measurements in whole blood confirmed a dominant role of Per2 for lactate production during myocardial ischemia. Surprisingly, high-throughput gene array analysis of eight different conditions on one 24-microarray plate revealed dominantly lipid metabolism as differentially regulated pathway in wildtype mice when compared to Per2-/-. In all treatment groups, the enzyme enoyl-CoA hydratase, which is essential in fatty acid beta-oxidation, was regulated in wildtype animals only. Studies using nuclear magnet resonance imaging (NMRI) confirmed altered fatty acid populations with higher mono-unsaturated fatty acid levels in hearts from Per2-/- mice. Unexpectedly, studies on gene regulation during reperfusion revealed solely pro inflammatory genes as differentially regulated 'Per2-genes'. Subsequent studies on inflammatory markers showed increasing IL6 or TNFa levels during reperfusion in Per2-/- mice. In summary, these studies reveal a novel role of cardiac Per2 for fatty acid metabolism or inflammation during myocardial ischemia and reperfusion. We pursued studies on Per2 dependent gene expression during myocardial ischemia or reperfusion to understand its impact on cardiac metabolism. We designed different ischemia and reperfusion protocols and performed a high-throughput expression profiling of 24 samples at a time using an industry-standard whole mouse gene array (Affymetrix, Mouse Gene 2.1 ST 24-Array). To understand differential gene regulation during different conditions we performed 1) 30 minutes of ischemia without reperfusion, 2) ischemic preconditioning (IP, 4 x 5 minutes ischemia and reperfusion), as known cardioprotective mechanism, and 3) 30 minutes of ischemia followed by 60 minutes of reperfusion. Based on three arrays per condition the total number of arrays was 24, which we analyzed at the same time on a multi plate array to avoid inter-array variations. Quality analysis using Partek Genomics Suite 6.6 revealed high confidence in the quality of the microarray data and all samples met 'Quality Assurance/Quality Control' (QA/QC) criteria.
2013-08-21 | E-GEOD-45818 | biostudies-arrayexpress
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
2011-02-19 | GSE20463 | GEO
Project description:We have sequenced miRNA libraries from human embryonic, neural and foetal mesenchymal stem cells. We report that the majority of miRNA genes encode mature isomers that vary in size by one or more bases at the 3’ and/or 5’ end of the miRNA. Northern blotting for individual miRNAs showed that the proportions of isomiRs expressed by a single miRNA gene often differ between cell and tissue types. IsomiRs were readily co-immunoprecipitated with Argonaute proteins in vivo and were active in luciferase assays, indicating that they are functional. Bioinformatics analysis predicts substantial differences in targeting between miRNAs with minor 5’ differences and in support of this we report that a 5’ isomiR-9-1 gained the ability to inhibit the expression of DNMT3B and NCAM2 but lost the ability to inhibit CDH1 in vitro. This result was confirmed by the use of isomiR-specific sponges. Our analysis of the miRGator database indicates that a small percentage of human miRNA genes express isomiRs as the dominant transcript in certain cell types and analysis of miRBase shows that 5’ isomiRs have replaced canonical miRNAs many times during evolution. This strongly indicates that isomiRs are of functional importance and have contributed to the evolution of miRNA genes
2014-08-06 | GSE58734 | GEO
Project description:To identify the role of mRNA during myocardial ischemia-reperfusion in mice, we have employed high-throughput sequencing to detect mRNA expression. Samples were collected from the control group and the ischemia reperfusion groups , with 5 samples per group. The candidate mRNA that may affect the process of myocardial ischemia-reperfusion was screened by comparing the ischemia-reperfusion group and the control group.
2023-11-15 | GSE223343 | GEO