Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Differentially expressed miRNAs in sepsis-induced acute kidney injury target oxidative stress and mitochondrial dysfunction pathways

ABSTRACT: Using the highly sensitive miRNA array, we screened 40 miRNAs were differentially expressed among the three groups and we explored the functions of these miRNAs in the serum by Gene Ontology and Kyoto Encyclopedia of Genes annotation. The enrichment results indicated that these miRNAs mainly participated in the oxidative stress and mitochondrial dysfunction pathways. Furthermore, the quantitative real-time polymerase chain reaction showed the different expression of miRNA might potentially be used to discriminate septic AKI from sepsis-non AKI and they were correlated with the regulation of mitochondrial oxidative stress and dysfunction, including PGC-1α, SIRT1, mTOR, OXSR1 and NOX5.

ORGANISM(S): Homo sapiens

PROVIDER: GSE94717 | GEO | 2017/02/10

SECONDARY ACCESSION(S): PRJNA373840

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Comprehensive Landscape of SA-AKI Revealed by Integrated Proteomics and Metabolomics Analysis

Project description:Sepsis-associated acute kidney injury (SA-AKI) is a severe and life-threatening condi-tion with high morbidity and mortality among emergency patients, and it poses a sig-nificant risk of chronic renal failure. Clinical treatments for SA-AKI remain reactive and non-specific, lacking effective diagnostic biomarkers or treatment targets. In this study, we established an SA-AKI mouse model using LPS and performed proteomics and metabolomics analyses. A variety of bioinformatic analyses, including Gene Set En-richment Analysis (GSEA), Weighted Gene Co-expression Network Analysis (WGCNA), protein and protein interactions (PPI), and MetaboAnalyst analysis, were conducted to investigate the key molecules of SA-AKI. Proteomics and metabolomics analyses re-vealed that sepsis led to impaired renal mitochondrial function and metabolic disorders. Immune-related pathways were found to be activated in kidneys upon septic infection. The catabolic products of polyamines accumulated in septic kidneys. Overall, our study provides a more comprehensive understanding of SA-AKI and identifies potential pathways for this condition.

2023-10-24 | PXD044371 | Pride

Differential RNA expression in kidney of mice with septic AKI induced by lipopolysaccharide

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

Transcriptome analysis of renal cortex from mice subjected to cecal ligation and puncture compared to control mice [RNA-seq]

Project description:Sepsis is a complex syndrome characterized by organ dysfunction triggered by dysregulated host response to infection, and the kidney is the most commonly injured organ. To model septic-induced AKI in animal, a well-established mouse model induced by caecal ligation and puncture (CLP) was established.

2023-11-09 | GSE220812 | GEO

CircRNA profile of renal cortex from mice subjected to cecal ligation and punture compared to control mice

2023-11-09 | GSE220782 | GEO

miRNA profiles of tubular cells (Rodent A and Rodent B)

Project description:MicroRNAs (miRNAs) are endogenous small RNAs of 18–23 nucleotides that regulate gene expression. Recently, plasma miRNAs have been investigated as biomarkers for various diseases. In the present study, we assessed whether the miRNA expression profiles of tubular tissues could discriminate proximal tubule injury and diagnose acute kidney injury (AKI) and the renal tubular dysfunction without morphological changes.

2015-03-17 | GSE66195 | GEO

miRNA profiles of tubular cells

2015-03-17 | GSE66134 | GEO

SIRT1 and H1AcK26 promoter-association in mouse ES cells changes upon oxidative stress

Project description:Association of the (histone) deacetylase SIRT1 with promoters was assessed to determine putative SIRT1-regulated genes. Based on the observation that the SIRT1 yeast ortholog Sir2 redistributes across the yeast genome in repsonse to genotoxic stress and double strand breaks (DSBs), we investigated the impact of oxidative stress on the chromatin binding pattern of SIRT1. Oxidative stress causes a major change in SIRT1 binding that is accompanied by an inverse H1K26 acetylation pattern. H1K26 was shown to be a direct target for deacetylation by SIRT1. Keywords: ChIP-chip, stress response

2008-11-26 | GSE13075 | GEO

Mouse urine proteome in case of septic AKI

Project description:Mouse urine proteome in case of septic AKI

2013-07-08 | PRD000453 | Pride

Homo sapiens

Project description:Differentially expressed miRNAs in sepsis-induced acute kidney injury target oxidative stress and mitochondrial dysfunction pathways

| PRJNA373840 | ENA

Proteomic analysis of septic renal acute phase response

Project description:Sepsis-induced acute kidney injury (AKI) is the most common form of AKI with poor outcomes. Renal proteomic analysis after bacterial lipopolysaccharide (LPS) administration revealed that the local renal acute phase reaction (APR) is one of the strongest responses of the kidney during septic AKI in mice. Evaluation of mRNA expression confirmed that most acute phase proteins were produced in the kidney. Our study also provides missing information on the time course of septic renal APR. Proteomic analysis of LPS-induced AKI demonstrated a marked upregulation of local renal acute phase response (APR) that commenced a few hours post injection and peaked at 24 h. Much more APPs were involved in the renal APR than previously identified.

2020-01-08 | PXD014664 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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