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Recombinant human thrombomodulin treatment against endotoxemia-induced myocardial injury

ABSTRACT: Recombinant human thrombomodulin treatment against endotoxemia-induced myocardial injury

PROVIDER: PRJNA543539 | ENA |

REPOSITORIES: ENA

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Recombinant human thrombomodulin treatment against endotoxemia-induced myocardial injury

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Single-cell RNA sequencing of liver parenchymal cells from murine model of endotoxemia

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Project description:Liver has a crucial role in the regulation of immune defense in systemic infections. During endotoxemia, the liver transits from an immune-tolerant towards an immune-active state and forms the first line of defense against invading microorganisms. the role of liver nonparenchymal cells in endotoxemia remains unintelligible. To characterize the liver nonparenchymal cells in endotoxemia liver, we performed single-cell RNA sequencing of liver nonparenchymal cells from healthy C57BL/6J mice and murine model of endotoxemia at early or late stage. The single-cell RNA-seq analyses revealed the heterogeneity of liver nonparenchymal cells in endotoxemia liver.

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Dabigatran protection against lipopolysaccharide induced endotoxemia is not mediated through its anticoagulant function

Project description:Endotoxemia is a key feature of sepsis pathogenesis and has also been found to mediate the pathophysiology of multiple chronic inflammatory conditions. In this work, we expand upon a model of endotoxemia due to lipopolysaccharide (LPS) using zebrafish and demonstrate that this model displays activation of inflammatory and pro-coagulant genes, impaired coagulation in response to endothelial injury, and signs of organ dysfunction. An in silico analysis revealed that there were multiple associations between the RNA-seq signature of LPS treated embryos and the RNA-seq signature of genes and drugs involving diverse pathways. An in vivo screen involving >1,500 FDA approved drugs identified multiple compounds spanning several drug categories that partially or completely prevented endotoxemic death. Three small molecules including one anticoagulant dabigatran were identified through both the in vivo and in silico analyses. Dabigatran, a direct thrombin inhibitor, significantly reduced the upregulation of inflammatory cytokines and pro-coagulant genes and completely protected zebrafish from endotoxemic death due to LPS. However, other anticoagulants argatroban (direct thrombin inhibitor), and rivaroxaban and apixaban, (factor Xa inhibitors), conferred no such protection. Lastly, prothrombin mutant fish displayed no increase in survival when treated with LPS. These data together suggest that dabigatran protects zebrafish from endotoxemia through a mechanism independent of its anticoagulant effect. In summary, our in silico and in vivo analyses reveals that dabigatran and several other novel small molecules prevent LPS induced endotoxemia and warrant further therapeutic exploration in inflammatory conditions, both acute and chronic.

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Dabigatran protection against lipopolysaccharide induced endotoxemia is not mediated through its anticoagulant function

Project description:Dabigatran protection against lipopolysaccharide induced endotoxemia is not mediated through its anticoagulant function

| PRJNA1027793 | ENA

RNA-seq of human adipose tissue following n-3 PUFA supplementation and evoked endotoxemia

Project description:Dietary consumption of long-chain omega-3 polyunsaturated fatty acids (n-3 PUFA) may protect against cardiometabolic disease through modulation of systemic and adipose inflammation. However, it is often difficult to detect the subtle effects of n-3 PUFA on inflammatory biomarkers in traditional intervention studies. We aimed to identify novel n-3 PUFA modulated gene expression using unbiased adipose transcriptomics during evoked endotoxemia in a clinical trial of n-3 PUFA supplementation. We analyzed adipose gene expression using RNA sequencing in the fenofibrate and omega-3 fatty acid modulation of endotoxemia (FFAME) trial of healthy individuals at three timepoints: before and after n-3 PUFA supplementation (n=8; 3600mg/day EPA/DHA) for 6weeks compared with placebo (n=6), as well as during a subsequent evoked inflammatory challenge (lipopolysaccharide 0.6ng/kg i.v.). As expected, supplementation with n-3 PUFA vs. placebo alone had only modest effects on adipose tissue gene expression. In contrast, the transcriptomic response to evoked endotoxemia was significantly modified by n-3 PUFA supplementation, with several genes demonstrating significant n-3 PUFA gene-nutrient interactions. These data highlight potential mechanisms whereby n-3 PUFA consumption may enhance the immune response to an inflammatory challenge.

2016-12-29 | GSE87426 | GEO

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