Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA137139 | ENA |
REPOSITORIES: ENA
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Project description:characterization of fibrinogen expression in the kidney, excretion in the urine following kidney damage and evaluating the therapeutic potential of fibrinogen in acute kidney injury. Total RNA was isolated of renal cortex and medulla from rats subjected to 20 min of bilateral ischemia followed by 6, 24 120, hr of reperfusion compared to sham rats.
2011-09-30 | E-GEOD-27274 | 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:The heart of late pregnant (LP) rodents is more prone to ischemia/reperfusion (I/R) injury compared to non-pregnant rodents. We hypothesized that Intralipid (ITLD) protects the heart in LP rodents against I/R injury. We performed genome-wide expression profiling to identify the underlying mechanisms. Female LP rat hearts were subjected to ischemia followed by reperfusion with vehicle or ITLD (one bolus of 5mg/kg).
2016-02-09 | E-GEOD-77698 | biostudies-arrayexpress
Project description:characterization of fibrinogen expression in the kidney, excretion in the urine following kidney damage and evaluating the therapeutic potential of fibrinogen in acute kidney injury.
2011-10-01 | GSE27274 | GEO
Project description:Female sex protects against development of acute kidney injury (AKI). While sex hormones may be involved in protection, the role of differential gene expression is unknown. We conducted gene profiling in male and female mice with or without kidney ischemia-reperfusion injury. Mice underwent bilateral renal pedicle clamping (30 min), and tissues were collected 24 hours after reperfusion. RNA-sequencing was performed on proximal tubules and kidney endothelial cells. Female mice were resistant to ischemic injury compared to males, determined by plasma creatinine, histologic scores, neutrophil infiltration, and extent of apoptosis. Sham mice had sex-specific gene disparities in proximal tubule and endothelium, and male mice showed profound gene dysregulation with ischemia-reperfusion compared to females. After ischemia proximal tubules from females exhibited smaller increases compared to males in injury-associated genes Lcn2, Havcr1, and Krt18, and no upregulation of Sox9 or Krt20. Endothelial upregulation of adhesion molecules and cytokines/chemokines occurred in males, but not females. Upregulated genes in male ischemic proximal tubules were linked to tumor necrosis factor and Toll-like receptor pathways, while female ischemic proximal tubules showed upregulated genes in pathways related to transport. The data suggest that sex-specific gene expression profiles in male and female proximal tubule and endothelium may underlie disparities in susceptibility to AKI.
2020-09-09 | GSE144622 | GEO
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:Ischemic preconditioning is effective in limiting subsequent ischemic acute kidney injury in experimental models. microRNAs are an important class of post-transcriptional regulator and show promise as biomarkers of kidney injury. An evaluation was performed of the time- and dose-dependent effects of ischemic preconditioning in a rat model of functional (bilateral) ischemia-reperfusion injury. A short, repetitive sequence of ischemic preconditioning resulted in optimal protection from subsequent ischemia-reperfusion injury. A detailed characterization of microRNA expression in ischemic preconditioning/ischemia-reperfusion injury was performed by small RNA-Seq.
2021-12-31 | E-MTAB-9896 | biostudies-arrayexpress
Project description:Ischemic preconditioning is effective in limiting subsequent ischemic acute kidney injury in experimental models. microRNAs are an important class of post-transcriptional regulator and show promise as biomarkers of kidney injury. An evaluation was performed of the time- and dose-dependent effects of ischemic preconditioning in a rat model of functional (bilateral) ischemia-reperfusion injury. A short, repetitive sequence of ischemic preconditioning resulted in optimal protection from subsequent ischemia-reperfusion injury. A detailed characterization of microRNA expression in ischemic preconditioning/ischemia-reperfusion injury was performed by Exiqon miRCURY microRNA array.
2021-12-31 | E-MTAB-9900 | biostudies-arrayexpress
Project description:Decorin protects cardiac myocytes against simulated ischemia/reperfusion injury
| PRJEB39277 | ENA
Project description:Ablation of macrophage transcriptional factor FoxO1 protects against ischemia-reperfusion injury-induced acute kidney injury
| PRJNA1054538 | ENA