Project description:To further explore the expression of circRNA, lncRNA and mRNA in mice with septic cardiomyopathy, we have employed microarray analysis as a discovery platform to identify circRNAs and lncRNAs with the potential to play role in the pathophysiology process of LPS-induced septic cardiomyopathy in mice. Six hours after intraperitoneal injection of LPS(10mg/kg) or saline solution, eight mice (LPS group, n=4; Cont group, n=4) were anesthetized and the heart were collected. And then total RNA was extracted and used for microarray detection.
Project description:Our previous work has focused on the relationship between non-coding RNAs and sepsis, so we chose to use microarray analysis to investigate the relationship between septic cardiomyopathy and a novel class of small non-coding RNA - tRNA-derived small RNAs(tsRNAs). Meanwhile, tRNA-derived small RNA has been studied in many cardiovascular diseases, but the relationship between tsRNAs and septic cardiomyopathy has not been investigated. We sought to analyze changes of tsRNAs expression profile in septic cardiomyopathy and reveal an important role for tsRNAs.
Project description:Septic cardiomyopathy (SCM) is the predominant cause of death in sepsis patients with undefined mechanism to date. Our study analyzed RNA sequencing (RNA-seq) data from rat heart tissue to discover key targets and potential pharmacological actions of the calcitonin gene-related peptide (CGRP) against SCM. A lipopolysaccharide-induced SCM model was established in rats (LPS 10 mg/kg, intraperitoneal (i.p.)). Thereafter, the myocardial tissues from the three groups of rats (Ctrl group, LPS group, and CGRP group) (n=5) were extracted and underwent RNA-seq, followed by bioinformatics analyses. Our findings suggest a basis for finding potential targets for CGRP in the treatment of SCM.
Project description:Our study helps to understand the molecular pathogenesis of septic cardiomyopathy in C57BL/6 mice and identifiy genes and pathways that may be potential therapeutic targets for septic cardiomyopathy treatment.
Project description:TLRs are considered important for innate immune responses that combat bacterial infections. Here, the role of TLRs in severe septic peritonitis using the colon ascendens stent peritonitis (CASP) model was examined. We demonstrate that mice deficient for MyD88 and TRIF had markedly reduced bacterial numbers both in peritoneal cavity and peripheral blood, indicating that bacterial clearance in this model is inhibited by TLR signals. Moreover, survival of Myd88-/-;TrifLps2/Lps2 mice was significantly improved. The lack of TLR signals prevented the excessive induction of inflammatory cytokines and of IL 10. Notably, the expression of IFN-gamma, which has an essential protective role in septic peritonitis, and of IFN-regulated genes including several p47 and p65 GTPases as well as IP 10 was independent of TLR signaling. These results provide evidence that, in severe septic peritonitis, TLR deficiency balances the innate immune response in a favorable manner by attenuating deleterious responses such as excessive cytokine release, while leaving intact protective IFN-gamma production. In this dataset, expression data of genes induced by septic peritonitis in spleens from TLR-deficient and wildtype mice are included. 3 groups (septic TLR-deficient mice, septic wildtype mice, and untreated wildtype mice) with 4 replicates each.
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.