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ABSTRACT:
PROVIDER: PRJNA1218621 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the therapeutic effect of Guanxinning injection (GXNI) on myocardial ischemia/reperfusion injury (MIRI) mice, we established MIRI model by ligating the left anterior descending (LAD) coronary artery of mice for 30 minutes and then reperfusion for 24 hours. We then performed RNA-seq on myocardial tissue of mice in the sham group, MIRI group and GXNI treatment group.
2022-09-27 | GSE214122 | GEO
Project description:The rats were subjected to left anterior descending (LAD) coronary artery ligation for 1 hour, 6 hours (MI1h and MI6h) and 24 hours (MI24h) along with Sham controls (Sham), and 1-hour, 6-hour ischemia followed by reperfusion (MI1h/R and MI6h/R, mimicking early time reperfusion (ETR) and late time reperfusion (LTR), respectively) followed by heart tissue collection 24 hours post MI to mimic the MI/R injury in AMI patients and pretreatment with FDA-approved PPARα agonist fenofibrate for each group.
2024-08-01 | GSE240847 | GEO
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:The rats were subjected to left anterior descending (LAD) coronary artery ligation for 1 hour, 6 hours (MI1h and MI6h) and 24 hours (MI24h) along with Sham controls (Sham), and 1-hour, 6-hour ischemia followed by reperfusion (MI1h/R and MI6h/R, mimicking early time reperfusion (ETR) and late time reperfusion (LTR), respectively) followed by heart tissue collection 24 hours post MI to mimic the MI/R injury in AMI patients.The heart infarct zones (Sham, MI1h/R, MI6h/R and MI24h) were isolated to single-nucleus transcriptome analysis. Collected nuclei for each sample were loaded onto 10X Chrominum platform. We obtained 22,234 cells and 17,003 genes. Five major cell types were identified, which included cardiomyocytes (CMs), endothelial cells (ECs), fibroblasts (FBs), macrophages (MACs) and smooth muscle cells (SMCs).
2024-08-01 | GSE240848 | GEO
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: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 | GSE72312 | GEO
Project description:Profile the microRNA expression in the Gracilis muscle of rat after 4h ischemia and 24 h reperfusion Following 4 h of ischemia and subsequent reperfusion for 4 h of the gracilis muscles, the specimens were analyzed with an Agilent rat miRNA array to detect the expressed miRNAs in the experimental muscles compared to those from the sham-operated controls. Two-condition experiment, Gracilis muscle after 4h ischemia and reperfusion injury for 24 h v.s. Gracilis muscle (sham control), Biological replicates: 2 control replicates, 2 experiement replicates
2010-04-22 | E-GEOD-21405 | biostudies-arrayexpress
Project description:Background: Ischemic preconditioning (IPC), i.e., brief periods of ischemia, protect the heart from subsequent prolonged ischemic injury, and reduces infarction size. Myocardial stunning refers to transient loss of contractility in the heart after myocardial ischemia that recovers without causing permanent damage. The relationship between IPC and myocardial stunning remains incompletely understood. Purpose: The primary aim of this study was to examine the effects of IPC on the relationship between ischemia duration, stunning, and infarct size in an ischemia-reperfusion injury model. The secondary aim of the study was to examine to which extent the phosphoproteomic changes induced by IPC relate to myocardial contractile function. Methods: Rats were subjected to different durations of left anterior descending artery (LAD) occlusion, with or without preceding IPC. Echocardiograms were acquired at 4 and 48 hours to assess cardiac contraction in the affected myocardial segment. Reversible akinesia was defined as the presence of myocardial akinesia at 4 hours that resolved by 48 hours; and was considered to represent myocardial stunning. Infarction size was evaluated using triphenyl tetrazolium chloride staining. Phosphoproteomic analysis was performed in heart tissue from preconditioned and non-preconditioned animals using nano-liquid chromatography-mass spectrometry. Results: Reversible akinesia was observed in a majority of the rats that were subjected to IPC and subsequently exposed to ischemia of 13.5 or 15 minutes of ischemia (83.3% [n/N] and 66.6% [n/N] respectively). Among rats without IPC, who were exposed to either 10, 11, 12 or 13.5 minutes of ischemia, reversible akinesia was observed in 0% (n/N), 17% (2/12), 0% (n/N) and 0% (n/N) of rats (p<0.001). Phosphoproteomic analysis revealed significant differential regulation of 809 phosphopeptides between IPC and non-IPC groups, with significant associations with the sarcomere, Z-disc, and actin binding. Conclusion: Our study shows that IPC preferentially induces changes in phosphosites of proteins involved in myocardial contraction, and both increases the incidence of reversible post-ischemic myocardial stunning after ischemia-reperfusion injury and reduces infarction size.
2024-05-15 | PXD050441 | Pride
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