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RNA sequencing of miRNA in plasma from myocardial ischemia and reperfusion mice and sham mice

ABSTRACT: RNA sequencing of miRNA in plasma from myocardial ischemia and reperfusion mice and sham mice

PROVIDER: PRJNA625985 | ENA |

REPOSITORIES: ENA

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RNA sequencing of miRNA in plasma from myocardial ischemia and reperfusion mice and sham mice

Project description:Purpose: The aim of this study is to compare the plasma miRNA profile between mice subject to myocardial ischemia and reperfusion and mice subject to sham operation. Methods: 8 to 10-week old C57BL/6 mice underwent myocardial ischemia and reperfusion (MIR) or Sham operation. Plasma RNA was isolated using Trizol LS reagent 4h post-surgery. NGS cDNA libraries were prepared using Norgen Biotek Small RNA Library Prep Kit. Library quality was validated prior to sequencing on an Illumina NextSeq 500 platform.

2020-04-18 | GSE148864 | GEO

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

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

CXCR1 and Its Downstream NF-κB Inflammation Signaling Pathway as a Key Target of Guanxinning Injection for Myocardial Ischemia/reperfusion Injury

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

Differential expression of mRNAs in the heart of ischemia-reperfusion mice

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

Vitamin B12 alleviates myocardial ischemia/reperfusion injury

Project description:To examine the protective effect of B12 on myocardial ischemia/reperfusion injury and figure out the mechanism of B12.

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phosphoproteome of hippocampus after focal cerebral ischemia 1.5 h and reperfusion 24 h in mice

Project description:We obtained the profiles of neuronal phosphoproteome after cerebral ischemia and reperfusion by isolating mice hippocampus. Hippocampus combined from either nine sham or nine focal cerebral ischemia 1.5 h and reperfusion 24 h (IR) mice were lysed, digested, labeled with different TMT tags, then pooled and analyzed by LC/LC-MS/MS. In total, we quantified 7,865 phosphopeptides,179 phosphorylation sites of 129 proteins were upregulated and 843 phosphorylation sites of 494 proteins were downregulated in hippocampus during cerebral ischemia 2 h compare with sham operation.

2024-02-15 | PXD033851 | Pride

Differential expression of cardiac mRNAs induced by Dexmedetomidine pretreatment in myocardial ischemia/reperfusion injury of mice

Project description:To investigate the cardioprotection of Dexmedetomidine, we established myocardial ischemia/reperfusion models in mice with vehicle or Dexmedetomidine pretreatment. We then performed mRNA sequencing of cardiac tissues and conducted gene expression profiling analysis.

2023-02-01 | GSE210873 | GEO

miRNA expression profile in intestinal ischemia reperfusion of adult mice

Project description:Intestinal ischemia/reperfusion (I/R) contributes to tissue damage, cellular apoptosis, systemic inflammatory responses, and even multiple organ dysfunction syndrome, however, underlying mechanisms remain unkown. In this report, we provide a comprehensive assessment of the expression of 1177 miRNAs on intestine tissues from mice suffering from sham and intestinal I/R. We find that 57 miRNA are up-regulated and 74 are down-regulated significantly. MiRNAs may be integral modulators of intestinal inflammation and enterocyte apoptosis associated with I/R and represent novel targets for future therapeutics. In the study, we profiled miRNA expression in the intestine from mice of 3 sham group and 3 intestinal ischemia/reperfusion group.

2016-06-25 | E-GEOD-83701 | biostudies-arrayexpress

Mesenchymal Stromal Cell-Derived Exosomes Attenuate Myocardial Ischemia-Reperfusion Injury through miR-182-Regulated Macrophage Polarization

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.

2021-09-01 | GSE120149 | GEO

Proteome of hippocampus after focal cerebral ischemia 1.5 h and reperfusion 24 h in mice

Project description:We obtained the profiles of neuronal proteome after cerebral ischemia and reperfusion by isolating mice hippocampus. Hippocampus combined from either nine sham or nine focal cerebral ischemia 1.5 h and reperfusion 24 h (IR) mice were lysed, digested, labeled with different TMT tags, then pooled and analyzed by LC/LC-MS/MS. In total, we quantified 5,059 proteins. We identified 142 differentially expressed proteins (t-test, p-value<0.05) after IR compared to sham groups. The results showed that 92 proteins were upregulated, and 50 proteins were downregulated after IR compared to sham groups. Gene ontology (GO) enrichment analysis of differentially expressed proteins between sham and IR groups. The results showed that the biological process of most of upregulated genes linked with immune inflammatory related responses were increased. And KEGG pathway analysis for upregulated genes showed that multiple immune inflammatory response pathways also increased significantly, such as TNF-signaling, NF-κB signaling and cytokine-cytokine receptor interaction, as well as NOD-like receptor signaling, and toll-like receptor signaling.

2024-02-15 | PXD033938 | Pride

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