Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

LncRNA and mRNA in a septic acute lung injury mouse model

ABSTRACT: Sepsis is commonly complicated by acute lung injury (ALI). We aimed to determine the long noncoding RNAs (lncRNAs) and mRNAs expression profiles in a cecal ligation and puncture mouse model of septic ALI. The model was verified by the elevation of inflammatory cytokine levels, the protein concentration in Bronchoalveolar lavage fluid and histological analysis of lung tissues. LncRNA and mRNA profiles were detected using an Agilent microarray. Bioinformatic analyses were employed to analyze the expression profiles and multiple biological functions. The results showed that lncRNAs These results implied that lncRNAs would be novel regulators and potential targets in septic ALI.

ORGANISM(S): Mus musculus

PROVIDER: GSE165226 | GEO | 2021/07/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data from lung of septic PPTA knockout mouse

Project description:In this study, we have explored microarray-based differential gene expression profile in mouse lung tissue 8 h after inducing polymicrobial sepsis and the effect of preprotachykinin-A (PPTA) gene deletion. A range of genes differentially expressed (> 2-fold) in microarray analysis was assessed, PPTA-knockout septic mice with their respective sham controls. We used microarrays to detail the global gene expression underlying sepsis in mice lacking the gene for substance P and identified distinct classes of up-regulated genes during this process. Lung samples from wild-type or PPTA-knockout mice were selected at 8 h after cecal ligation and puncture (CLP) or sham surgery for RNA extraction and hybridization to Affymetrix microarrays. Triplicates were performed for each condition.

2010-03-15 | E-GEOD-15379 | biostudies-arrayexpress

Lung Tissue Exosome-Mediated Delivery of ceRNA Networks as a Novel Mechanism for Sepsis-induced Acute Lung Inflammation (miRNA-Seq)

Project description:Acute lung injury (ALI) is associated with a high mortality rate; however, the underlying molecular mechanisms are poorly understood. The purpose of this study was to investigate the expression profile and related networks of long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and mRNAs in lung tissue exosomes obtained from sepsis-induced ALI. A mouse model of sepsis was established using the cecal ligation and puncture method. RNA sequencing was performed using lung tissue exosomes obtained from mice in the sham and CLP groups. Hematoxylin-eosin staining, western blotting, immunofluorescence, quantitative real-time polymerase chain reaction, and nanoparticle tracking analysis were performed to identify relevant phenotypes, and bioinformatic algorithms were used to evaluate competitive endogenous RNA (ceRNA) networks.Thirty lncRNA-miRNA-mRNA interactions were identified, including two upregulated lncRNAs, 30 upregulated miRNAs, and two downregulated miRNAs. Based on the expression levels of DEmRNAs, DELncRNAs, and DEmiRNAs, 30 ceRNA networks were constructed. This study revealed, for the first time, biomarkers of lung tissue exosome RNA and the related networks of lncRNA in sepsis-induced ALI. We revealed a novel molecular mechanism of sepsis-induced ALI, which may support the diagnosis and treatment of sepsis-induced ALI.

2023-12-31 | GSE227365 | GEO

Lung Tissue Exosome-Mediated Delivery of ceRNA Networks as a Novel Mechanism for Sepsis-induced Acute Lung Inflammation (lncRNA-Seq)

2023-12-31 | GSE227364 | GEO

The role and mechanism of R-spondin3 in pulmonary vascular barrier dysfunction induced by mechanical ventilation

Project description:To investigate the effect of lowl tidal volume (LV) ventilation on the pathological development of severe lung injury, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to influence LV-induced lung injury. A mouse model of septic lung injury induced by cecal ligation and puncture was conducted, 24 h post-CLP,mice were exposed to LV (6ml/kg) for 12h

2023-03-15 | GSE226807 | GEO

IL-36 receptor deletion aggravates lung injury and mortality in experimental murine sepsis through epithelial

Project description:Inflammation resolution is critical for sepsis induced acute lung injury (ALI) recovery. Interleukin-36 receptor (IL-36R) is a potent anti-inflammatory factor. However, its role in ALI resolution remains unclear. We investigated the effects of IL-36R during the ALI resolution process in a murine cecal ligation and puncture (CLP)-induced ALI model. Knockout IL-36R signaling aggravates CLP-induced lung injury, as manifested by elevated bacterial load and increased neutrophils recruitment to the lung. Thereafter, we used IL-36R knockout mice to discern the source cell of IL-36R during ALI. We found that IL-36R is predominantly generated by epithelial cells during the ALI process. Furthermore, we sorted lung epithelial cells on the ALI process. IL-36R-specific loss in epithelial cells leads to apoptosis through NF-κB pathway. Together, our findings identify molecules that are likely involved in sepsis induced lung injury that may inform biomarker and therapeutic development.

2024-01-02 | GSE240924 | GEO

Gene expression profiling in lung tissues of an animal model of sepsis-induced acute lung injury

Project description:Gene expression profiling was performed in lung tissues from an animal model of sepsis challenged with injurious and non-injurious mechanical ventilation to unravel the molecular pathways involved in acute lung injury. Sepsis was induced in male Sprague Dawley rats by means of cecal ligation and puncture. Septic rats were randomly allocated to three distinct groups: spontaneous breathing, mechanically ventilated with high tidal volume with zero positive end expiratory pressure (PEEP) and with low tidal volume and 10 cmH2O of PEEP. Comparisons were performed against an unventilated control group.

2015-07-01 | E-MTAB-2673 | biostudies-arrayexpress

Antigen-presenting aged neutrophils induce CD4+ T cells to exacerbate inflammation in sepsis

Project description:Extracellular cold-inducible RNA-binding protein (eCIRP) is a key mediator of severity and mortality in sepsis. We found that stimulation of mouse bone marrow–derived neutrophils (BMDNs) with eCIRP generated a distinct neutrophil subpopulation, characterized by cell surface markers of both antigen-presenting cells and aged neutrophils as well as expression of IL-12, which we named antigen-presenting aged neutrophils (APANs). The frequency of APANs was significantly increased in the blood, spleen, and lungs of WT mice subjected to cecal ligation and puncture–induced sepsis but not in CIRP–/– mice. Patients with sepsis had a significant increase in circulating APAN counts compared with healthy individuals. Compared with non–APAN-transferred mice, APAN-transferred septic mice had increased serum levels of injury and inflammatory markers, exacerbated acute lung injury (ALI), and worsened survival. APANs and CD4+ T cells colocalized in the spleen, suggesting an immune interaction between these cells. APANs cocultured with CD4+ T cells significantly induced the release of IFN-γ via IL-12. BMDNs stimulated with eCIRP and IFN-γ underwent hyper-NETosis. Stimulating human peripheral blood neutrophils with eCIRP also induced APANs, and stimulating human neutrophils with eCIRP and IFN-γ caused hyper-NETosis. Thus, eCIRP released during sepsis induced APANs to aggravate ALI and worsen the survival of septic animals via CD4+ T cell activation, Th1 polarization, and IFN-γ–mediated hyper-NETosis.

2023-09-27 | GSE228482 | GEO

Integrated lncRNAs and mRNAs sequencing reveals lncRNAs regulatory network associated with lung injury in LPS-induced septic shock rats

Project description:Sepsis is associated with increased morbidity and mortality. Long non-coding RNAs (lncRNAs) have been associated with human diseases. Here, we used a microarray to analyze lncRNAs and mRNAs expression and functional network of lung injury in lipopolysaccharide (LPS)-induced septic shock rats.

2023-07-17 | GSE154653 | GEO

Hydrogen gas therapy attenuate inflammatory pathway signaling in septic mice

Project description:Molecular hydrogen (H2) has been used in several clinical cases. However, few studies have been reported on the use of hydrogen therapy for treatment of sepsis, and the anti-inflammatory mechanism of H2 remains majorly unknown. The aim of this study is to confirm the effects of H2 therapy for sepsis and reveal its therapeutic mechanism by performing RNA-seq in multiple organs in the septic mice. Nine-week-old C57BL/6 male mice underwent cecal ligation and puncture procedure (CLP) or sham procedure. Subsequently, the CLP model received an immediate +/- continuous inhalation of 7% H2. The H2 gas-treated groups were housed in the same cage, and they were put in a designated box that was able to maintain the concentration of H2 through constant H2 supply by a gas generator. Mice were observed for a week to assess their survival rates. Serum inflammatory cytokines were evaluated with ELISA at 24 h after the CLP procedure.

2021-02-28 | GSE152527 | GEO

Genetic deletion of translocator protein exacerbates post-sepsis syndrome with activation of the C1q pathway in septic mouse model

Project description:To investigate the role of TSPO in the sequelae of sepsis induced by cecal ligation and puncture (CLP), hippocampal gene expression changes after CLP surgery were examined in wild-type and TSPO KO mice

2023-01-01 | GSE220153 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data