Expression data from mouse heart tissue ischemia/reperfusion (I/R) treated for 0,24,48,72 hours
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ABSTRACT: Myocardial Ischemia-reperfusion injury is a serious clinical problem that lacks effective therapy.However, the precise mechanism leading to myocardial I/R injury remains unclear.Our study defined the dynamic changes of the differentially expressed genes related myocardial I/R injury, and provide basis for comprehensive understanding of the disease at molecular level. We investigated schemia-reperfusion –mediated gene expression alteration associated with the development of cardiac injury by microarray in a mouse model.
Project description:Myocardial Ischemia-reperfusion injury is a serious clinical problem that lacks effective therapy. However, the precise mechanism leading to myocardial I/R injury remains unclear.Our study defined the dynamic changes of the differentially expressed genes related myocardial I/R injury, and provide basis for comprehensive understanding of the disease at molecular level. We investigated schemia-reperfusion –mediated gene expression alteration associated with the development of cardiac injury by RNA-seq in a mouse model.
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)
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.
Project description:Aims: Mesenchymal stem cells (MSCs) gradually become attractive candidates for cardiac inflammation modulation, yet understanding of the mechanism remains elusive. Strikingly, recent studies indicated that exosomes secreted by MSCs might be a novel mechanism for the beneficial effect of MSCs transplantation after myocardial infarction. We therefore explored the role of MSC-derived exosomes (MSC-Exo) in the immunomodulation of macrophages after myocardial ischemia-reperfusion and its implications in cardiac injury repair. Methods and Results: Exosomes were isolated from the supernatant of MSCs using a gradient centrifugation method. Administration of MSC-Exo through intramyocardial injection after myocardial ischemia reperfusion reduced infarct size and alleviated inflammation level in heart and serum. Systemic depletion of macrophages with clodronate liposomes abolished the curative effects of MSC-Exo. MSC-Exo modified the polarization of M1 macrophages to M2 macrophages both in vivo and in vitro. miRNA-sequencing of MSC-Exo and bioinformatics analysis implicated miR-182 as a potent candidate mediator of macrophage polarization and TLR4 as a downstream target. Diminishing miR-182 in MSC-Exo partially attenuated its modulation of macrophage polarization. Likewise, knock down of TLR4 also conferred cardioprotective efficacy and reduced inflammation level in a mouse model of myocardial ischemia/reperfusion. Conclusion: Our data indicates that MSC-Exo attenuates myocardial ischemia/reperfusion injury via shuttling miR-182 that modifies the polarization state of macrophages. This study sheds new light on the application of MSC-Exo a potential therapeutic tool for myocardial ischemia/reperfusion injury.
Project description:Acute myocardial infarction remains a leading cause of morbidity and mortality worldwide. Our previous studies have investigated the role of the transcription factor Kruppel-like factor 5 (KLF5) in various cardiac disease models, including diabetic cardiomyopathy and ischemic heart failure, and have linked it to the regulation of cellular stress responses, particularly those associated with oxidative stress and metabolic dysregulation. This study examines the role of KLF5 in exacerbating myocardial ischemia/reperfusion (I/R) injury and explores the potential cardioprotective benefit of KLF5 inhibition. Using the surgical model of myocardial I/R injury in both pigs and mice, we observed that KLF5 expression is upregulated in cardiomyocytes during early reperfusion. This increase in KLF5 expression is accompanied by enhanced oxidative stress, apoptosis, fibrosis, and adverse cardiac remodeling. Pharmacologic and cardiomyocyte-specific genetic inhibition of KLF5 significantly reduced infarct size, oxidative stress, and cell apoptosis markers, while preserving cardiac function over both acute and long-term reperfusion periods.
Project description:This SuperSeries is composed of the following subset Series: GSE21405: MicroRNA Profiling In Ischemia-Reperfusion Injury Of The Gracilis Muscle In Rats GSE21406: Potential Target Genes of MicroRNA-21 In Ischemia-Reperfusion Injury Of The Gracilis Muscle In Rats Refer to individual Series
Project description:Ischemia reperfusion injury (IRI) in organ transplantation remains a significant problem with limited alternative therapeutic options. Organs that undergo significant damage during IRI, particularly those enduring long warm ischemia times, undergo significant delayed graft function (DGF) after reperfusion and tend to have greater complications long term with the onset of chronic rejection. The gas molecule carbon monoxide (CO) has emerged as an agent that can suppress IRI in rodent models of solid organ transplantation. Since the use of CO is a potential therapeutic modality in humans, we tested if CO can prevent DGF in a pig model of kidney transplantation Keywords: stress response, treatment response 18 Samples from pig kidneys, two naïve controls, two timepoints, two conditions, 4 replicates
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.