Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1256764 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR33367051_1.fastq.gz | Fastqsanger.gz | |||
| SRR33367051_2.fastq.gz | Fastqsanger.gz | |||
| SRR33367052_1.fastq.gz | Fastqsanger.gz | |||
| SRR33367052_2.fastq.gz | Fastqsanger.gz | |||
| SRR33367053_1.fastq.gz | Fastqsanger.gz |
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Project description:Background: Sepsis can lead to multiple organ damage, and the heart is one of the most vulnerable organs. Vagal nerve stimulation can reduce myocardial injury in sepsis and improve survival rate. However, the relative effect of disparate cell populations on sepsis induced myocardial dysfunction and the low-level tragus stimulation on it, remain unclear. Methods: We used the cardiac single-cell transcriptomic strategy to characterize the cardiac cell population and the network of cells that forms the heart. And we selected all cardiac macrophage from CD45+ cells using single-cell mRNA sequencing data. Then we used echocardiography performing, western blot and immunofluorescence and immunohistochemical technology to verify the data of the single-cell mRNA sequencing results. Results: In single-cell mRNA sequencing data, our analysis provides a comprehensive map of the cardiac cellular landscape uncovering multiple cell populations that contribute to sepsis induced myocardial dysfunction under low-level tragus stimulation. Pseudo timing analysis in single-cell sequencing showed that low level vagal nerve stimulation could induce the transformation of cardiac monocytes into M2 macrophages and play an anti-inflammatory role. After low-level tragus stimulation, the expression of α7nAChR in the heart tissue increased significantly. Echocardiography showed that low-level tragus stimulation could improve the cardiac function of septic myocardial injury of the mice. Comparing with the sepsis group, the expression of interleukin-1β in heart tissue of the mice in sepsis with low-level tragus stimulation group is significantly lower. Conclusion: Low-level tragus stimulation can improve sepsis-induced myocardial dysfunction by promoting cardiac monocytes to M2 macrophages. Goal of the study: In the present study, we aimed to screen macrophages, their crosstalk with other cells, and macrophages associated with cardiac injury and further verify their origins and roles in the septic myocardial injury process and low-level tragus stimulation (LL-TS) to treat septic myocardial dysfunction.
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Project description:Transcriptional profiling of Biomphalaria snail (whole body tissues) comparing BS90 strain untreated with sterile wounding and septic injury using a new comprehensive microarray platform design. Goal was to compare responses to differen immune challenges within one strain. Three-condition experiment one strain untreated vs. injury vs. septic injury, Biological replicates: 2 control replicates, 3 injured replicates, 2 septic injury replicates.
2016-07-30 | E-GEOD-71054 | biostudies-arrayexpress
Project description:Nowadays, sepsis and septic shock have become major public health problems, which are the main cause of death among patients admitted to the intensive care units. Notably, myocardial dysfunction during sepsis, usually called sepsis-induced myocardial depression, is common in septic shock patients whose incidence is about 70% and leads to a high mortality. However, the mechanism underlying the septic myocardial depression is still unclear. Recently, proteomics has become a powerful method for explore protein dynamics and their complex regulatory mechanism, and thus generates a profound impact on precision medicine and the clinical setting. Importantly, the expression patterns of global proteins in heart tissue between sepsis and control group remain unclear. Therefore, we performed the rat models of sepsis-induced myocardial depression and investigated global protein expression profiles in heart tissue between sepsis and control group using 4D label-free proteomic technique.
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Project description:Drosophila 3rd instar larvae were subjected to septic injury. After 6h plasmatocytes were isolated, fixed and subjected to ChIP-seq.
2022-05-31 | E-MTAB-10760 | biostudies-arrayexpress
Project description:Sepsis is a life-threatening disease that often causes multiple organ dysfunctions. Long noncoding RNAs (lncRNAs) are involved in the pathogenesis and development of sepsis. However, there is little known about the function of lncRNAs in sepsis-induced myocardial dysfunction.To test the hypothesis that dysregulating lncRNAs may be involved in sepsis-induced myocardial dysfunction, we identified differentially expressed (DE) lncRNAs and mRNAs in cardiac tissue by high-throughput sequencing. We constructed coding and non-coding co-expression (CNC) and lncRNA-micro RNA (miRNA)-mRNA competing endogenous networks. The findings will provide useful information for exploring therapeutic candidate targets and new molecular biomarkers of septic myocardial injury.
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Project description:Since septic AKI is a common type of AKI in ICU, we need to understand the differences in renal RNA expression in septic kidney injury. Therefore, we used lipopolysaccharide intraperitoneal injection to construct a mouse model of septic renal injury, and verified that the model was successful, then RNA sequencing was performed. To know the difference of RNA expression through the comparison of kidney sequencing between the normal group and the septic AKI group.
2023-04-03 | GSE227623 | GEO
Project description:Septic cardiac dysfunction is a key feature of severe sepsis and septic shock, contributing to multiorgan dysfunction syndrome and death. It has been established that persistent beta adrenergic stimulation is detrimental in sepsis, and that specific beta 1 blockade mitigates excessive systemic inflammation and improves myocardial function. The aim of this study was to investigate the effects of specific beta 1 blocker esmolol on septic mouse myocardium by genomic and proteomic techniques. We also evaluated survival of septic mice and systemic inflammation under esmolol treatment.
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Project description:Recent evidence has shown that long non-coding (lncRNA) rPvt1 is elevated in septic myocardial tissues, and knockdown of rPvt1 attenuates the sepsis induced myocardial injury. However, the mechanisms of rPvt1 in septic myocardial dysfunction have still not been illustrated. In this study, we carried out transcriptomic, proteomic and metabolomic assays, and conducted an integrated multi-omics analysis to explore the associations of rPvt1 in a lipopolysaccharide (LPS)-induced H9C2 cardiomyocyte injury. Silencing of rPvt1 was achieved via a lentivirus transduction system. Compared to the negative control, rPvt1 knockdown lead to large changes on the transcriptome, proteome and metabolome. 2385 differentially expressed genes (DEGs), 272 differentially expressed proteins (DEPs) and 75 differentially expressed metabolites (DEMs) were identified by each omics respectively. Gene Ontology (GO) functional annotation, Kyoto Encyclopedia of Genes and Genomes (KEGG), Nr, eukaryotic orthologous groups (KOG) and clusters of orthologous groups of proteins (COG) pathway analysis was conducted on these differentially expressed factors. The results suggest that mitochondrial energy metabolism may be a closely related mechanism by which Pvr1 links. These genes, proteins and metabolites and their related dysregulated pathways may become promising targets for the studies on investigating the rPvt1-regluatory mechanisms in septic myocardial dysfunction, which is important for formulating novel strategies on the prevention, diagnosis, and treatment of septic myocardial injury.
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Project description:Trained immunity is classically characterized by long-term epigenetic reprogramming of innate immune cells to combat infectious diseases. Infection-induced organ injury is a common clinical severity phenotype of sepsis. However, whether the induction of trained immunity plays a role in protecting septic-organ injury remains largely unknown. Here, through establishing an in vivo β-glucan training and secondary LPS challenge-induced organ injury model in zebrafish larvae, we observe that induction of trained immunity could inhibit the pyroptosis of hepatocytes to alleviate septic-liver injury, with an elevated epigenetic modification of trimethylation at histone 3 lysine 4 (H3K4me3) that targets mitophagy activation. Moreover, we identify a novel C-type lectin domain receptor in zebrafish, named DrDectin-1, which is revealed as the orchestrator in gating H3K4me3 rewiring-mediated mitophagy activation and alleviating the pyroptosis-engaged septic-liver injury in vivo. Taken together, our results uncover a tissue-resident trained immunity in maintaining tissue homeostasis at a whole animal level, and offer a facile in vivo model to efficiently integrate trained immunity for immunotherapies.
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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.
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