The present study aimed to analyze long noncoding RNA (lncRNA) and messenger RNA (mRNA) expression profiles in septic mice heart and to identify potential lncRNAs and mRNAs that be responsible for cardiac mitochondrial dysfunction during sepsis. Mice were treated with 10 mg/kg of lipopolysaccharides to induce sepsis. LncRNAs and mRNAs expression were evaluated by using lncRNA and mRNA microarray or real-time polymerase chain reaction technique. LncRNA-mRNA coexpression network assay, Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed. The results showed that 1275 lncRNAs were differentially expressed in septic myocardium compared with those in the control group. A total of 2769 mRNAs were dysregulated in septic mice heart, most of which are mainly related to the process of inflammation, mitochondrial metabolism, oxidative stress, and apoptosis. Coexpression network analysis showed that 14 lncRNAs were highly correlated with 11 mitochondria-related differentially expressed mRNA. Among all lncRNAs and their cis-acting mRNAs, 41 lncRNAs-mRNA pairs (such as NONMMUG004378 and Apaf1 gene) were enriched in GO terms and KEGG pathways. In summary, we gained some specific lncRNAs and their potential target mRNAs that might be involved in mitochondrial dysfunction in septic myocardium. These findings provide a panoramic view of lncRNA and might allow developing new treatment strategies for sepsis.
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http://dx.doi.org/10.1002/jcb.29831 | DOI Listing |
Eur J Med Res
January 2025
Infectious Diseases Department, Jinhua Central Hospital, Jinhua, 321000, China.
Background: Sepsis is characterized by an excessive immune response. Modulation of the immune response, particularly macrophage polarization, may provide therapeutic benefit. The effects of Caerulomycin A (caeA), a known STAT1 phosphorylation inhibitor, on macrophage polarization and inflammatory markers were explored using a lipopolysaccharide (LPS)-induced sepsis mouse model.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Department of Critical Care Medicine, West China Hospital, Sichuan University, China. Electronic address:
Background: Sepsis is defined as multi-organ dysfunction caused by dysregulated host response to infection. This dysregulated host response includes enhanced inflammatory responses and suppressed adaptive immunity, but the molecular mechanisms behind it have not yet been elucidated. CD72, a type II transmembrane protein that is primarily expressed in B cells, was found to play an immunomodulatory role in the immune system and was associated with mortality in patients with sepsis.
View Article and Find Full Text PDFAllergol Immunopathol (Madr)
January 2025
Department of Pediatrics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zheiiang, China.
To illustrate the potential of mesenchymal stem cell-derived exosomes (MSC-Exos) in mitigating septic lung injury by reducing the excessive formation of neutrophil extracellular traps (NETs), a mouse model of septic lung injury was induced through cecal ligation and puncture (CLP). The mice received intraperitoneal injections of MSC-Exos. Post injection, pathological alterations of the lung tissue were evaluated through HE staining, and the levels of inflammatory markers in each mouse group at various time points were assessed using ELISA kits.
View Article and Find Full Text PDFFASEB J
January 2025
Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Neutrophils are peripheral blood-circulating leukocytes that play a pivotal role in host defense against bacterial pathogens which upon activation, they release web-like chromatin structures called neutrophil extracellular traps (NETs). Here, we analyzed and compared the importance of myeloid differentiation factor 88 (MYD88), peptidyl arginine deiminase 4 (PAD4), and gasdermin D (GSDMD) for NET formation in vivo following sepsis and neutrophilia challenge. Injection of lipopolysaccharide (LPS)/E.
View Article and Find Full Text PDFAdv Mater
January 2025
State Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, Tianjin, 300350, China.
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