RNA sequencing on the infarct zone after ischemia reperfusion (I/R)
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PROVIDER: PRJNA642843 | ENA |
REPOSITORIES: ENA
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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:Hearts received a sham or an I/R surgery. After indicated timepoints, the infarct region was isolated and used for RNA sequencing
2020-06-30 | GSE153493 | GEO
Project description:Calcium/calmodulin-dependent protein kinase II (CaMKII) was suggested to mediate ischemic myocardial injury and adverse cardiac remodeling. However, the specific functions of the CaMKII isoforms and splice variants in ischemia/reperfusion (I/R) injury have not been investigated yet. Thus, we studied the roles of the CaMKII isoforms and splice variants in I/R by the use of various CaMKII mutant mice. CaMKIIδC was up-regulated already one day after I/R injury but surprisingly, acute I/R injury was neither affected in CaMKIIδ-deficient mice, CaMKIIδ-deficient mice in which the splice variants CaMKIIδB and C were re-expressed nor in conditional CaMKIIδ/γ double-knockout mice (DKO). In contrast, 5 weeks after I/R, DKO mice were protected against extensive scar formation and cardiac dysfunction. Leukocyte infiltration was not altered one day but five days after I/R, explaining the late effects of CaMKII deletion on post-I/R remodeling. Other than reported before, we demonstrate that CaMKII is not critically involved in the immediate mechanisms that regulate acute I/R injury but in the process of post-infarct remodeling. We analysed 6 groups in total: 3 groups from wild-type control animals and 3 groups from CaMKII delta/gamma double-KO mice. Sham operated animals served as controls in both wild-type and KO animal groups. 2 different time points in ischia/reperfusion operated animals were investigated: 1 day and 5 days post-surgery.
2014-09-08 | E-GEOD-58486 | biostudies-arrayexpress
Project description:LncRNA and mRNA profiling of the ischemia zone, the border zone and the remote non-ischemia zone of murine myocardial ischemia/reperfusion (MI/R) hearts
| PRJNA675764 | ENA
Project description:RNA-sequencing of the infarct border zone of the mouse hearts transplanted with FOXO3-GE-MPCs
2020-04-30 | GSE149594 | GEO
Project description:Calcium/calmodulin-dependent protein kinase II (CaMKII) was suggested to mediate ischemic myocardial injury and adverse cardiac remodeling. However, the specific functions of the CaMKII isoforms and splice variants in ischemia/reperfusion (I/R) injury have not been investigated yet. Thus, we studied the roles of the CaMKII isoforms and splice variants in I/R by the use of various CaMKII mutant mice. CaMKIIδC was up-regulated already one day after I/R injury but surprisingly, acute I/R injury was neither affected in CaMKIIδ-deficient mice, CaMKIIδ-deficient mice in which the splice variants CaMKIIδB and C were re-expressed nor in conditional CaMKIIδ/γ double-knockout mice (DKO). In contrast, 5 weeks after I/R, DKO mice were protected against extensive scar formation and cardiac dysfunction. Leukocyte infiltration was not altered one day but five days after I/R, explaining the late effects of CaMKII deletion on post-I/R remodeling. Other than reported before, we demonstrate that CaMKII is not critically involved in the immediate mechanisms that regulate acute I/R injury but in the process of post-infarct remodeling.
2014-09-08 | GSE58486 | 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: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
Project description:Ischemic heart failure after acute myocardial infarction (AMI) is a major cause of morbidity and mortality worldwide. We recently reported that activation of a trans-valvular axial-flow pump in the LV and delaying myocardial reperfusion, known as Primary Unloading, limits infarct size by reducing LV wall stress and increasing expression of the cardioprotective cytokine, stromal derived factor 1 alpha (SDF1a). The mechanisms underlying the cardioprotective benefit and sustained effect of Primary Unloading remain poorly understood. We now tested the importance of delayed reperfusion, the functional significance of SDF1a, and the late-term impact on myocardial function and scar size associated with Primary Unloading. Adult male swine were subjected to Primary Reperfusion or Primary Unloading after 90 minutes of left anterior descending artery occlusion. Compared to Primary Reperfusion, 30 minutes of Primary Unloading was necessary and sufficient prior to reperfusion to limit infarct size. Primary Unloading was associated with a global shift in gene expression within the infarct zone favoring cardioprotection. Compared to Primary Reperfusion, Primary Unloading for 30 minutes preserved SDF1a protein levels without changing SDF1a mRNA levels within the infarct zone and further promoted a shift towards anti-apoptotic signaling within the infarct zone. Primary Unloading reduced activity levels of proteases known to degrade SDF1a and blocking the SDF1a receptor, CXCR4, attenuated the cardioprotective effect of Primary Unloading. Primary Unloading further reduced LV scar size, improved cardiac function, limited expression of markers associated with heart failure and maladaptive remodeling within the non-infarct zone 28 days after acute myocardial infarction. In conclusion, we introduce that Primary Unloading for 30 minutes before, not after reperfusion limits infarct size, increases SDF1a levels within the infarct zone, and results in a durable reduction in LV scar size, improved cardiac function, and limits markers of heart failure and maladaptive remodeling 28 days after AMI.
2018-10-25 | GSE108644 | GEO
Project description:NRVMs were subjected to varying durations of ischemia or ischemia+reperfusion using coverslip hypoxia. Expression profiling was used to identify genes that are differentially regulated in either event. We used microarrays to detail the global program of gene expression underlying ischemia and reperfusion using Coverslip Hypoxia and identified distinct classes of genes regulated during these processes. Experiment Overall Design: RNA was extracted from NRVMs subjected to varying durations of ischemia or ischemia+reperfusion and hybridized to rat genome Affymetrix arrays.
2008-06-15 | E-GEOD-6701 | biostudies-arrayexpress