Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profile of kidney and lung cells at 24 hours after the onset of renal bilateral ischemia-reperfusion injury

ABSTRACT: Remote lung injury after acute kidney inkury (AKI) is a common issue in humans and is lethal especially in critically-ill patients. We investigated kidney-lung interactions following AKI using single-cell RNA sequencing (scRNA-seq) of kidney and lung in a murine AKI model.

ORGANISM(S): Mus musculus

PROVIDER: GSE249928 | GEO | 2025/02/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Glutamine attenuates renal ischemia-reperfusion injury and prevents acute kidney damage

Project description:Acute kidney injury (AKI) represents a common complication in critically ill patients that is associated with an increased morbidity and mortality. Currently, no effective treatment options are available. Here, we show that glutamine significantly attenuates leukocyte recruitment and inflammatory signaling in human and murine tubular epithelial cells (TECs). In a murine AKI model induced by ischemia-reperfusion-injury (IRI) we show that glutamine causes transcriptomic and proteomic reprogramming in renal TECs and neutrophils, resulting in decreased epithelial apoptosis, neutrophil recruitment and improved mitochondrial functionality and respiration provoked by an ameliorated oxidative phosphorylation. We identify the proteins glutamine gamma glutamyltransferase 2 (Tgm2) and apoptosis signal-regulating kinase (Ask1) as the major targets of glutamine in apoptotic signaling. Increased Tgm2 expression and reduced Ask1 activation result in decreased JNK activation leading to a diminished mitochondrial intrinsic apoptosis in kidneys upon IRI-induced AKI and under hypoxia or following TNFα-treatment of TECs. Consequently, glutamine administration attenuated kidney injury in vivo during AKI progression as well as TEC viability in vitro under inflammatory and hypoxic conditions.

2023-03-11 | PXD029723 | Pride

Transcriptome profile of a murine renal bilateral ischemia reperfusion model 2 hours to 12 months post injury

Project description:Acute kidney injury (AKI) is associated with an increased risk of chronic kidney disease (CKD). To extend our understanding of renal repair, and its limits, we performed a detailed molecular characterization of a murine ischemia reperfusion injury (IRI) model for 12 months post injury. RNA-seq analysis highlights a cascade of temporal specific gene expression patterns related to tubular injury/repair, fibrosis, innate and adaptive immunity.

2017-09-12 | GSE98622 | GEO

Blockade of TNFα after ischemia reperfusion injury ameliorates renal prognosis

Project description:Recently, acute kidney injury (AKI) is thought to develop a predisposition toward chronic kidney disease. But the detailed mechanism of the disease progression after AKI is unknown. We made two ischemia-reperfusion injury (IRI) mice models, repaired kidney model and atrophic kidney model, and studied the mechanism that kidney after IRI became atrophy. We found that the atrophy kidney model had two peaks of apoptosis 3 and 14 days after IRI, whereas the repaired kidney model had only one apoptosis peak 3 days after IRI. We showed that the second apoptosis is responsible for the kidney atrophy. Moreover, apoptotic ligands, TNFα and FasL were upregulated at the same time of two apoptosis peaks on the atrophic kidney, and blockade of them before IRI prevented kidney from falling into atrophy. Surprisingly, inhibition of the second apoptosis by anti-TNFα antibody protected from renal atrophy. We propose that apoptosis might play a major role in AKI progression and blockade of TNFα after IRI will be a new therapeutic approach for AKI.

2012-08-10 | GSE39766 | GEO

Expression data from kidneys of male EST KO mice in comparison to kidneys of male wild type mice subjected to warm bilateral renal artery ischemia-reperfusion injury

Project description:EST KO mice are protected from ischemic acute kidney injury (AKI). Many genes were shown to be altered in this group.

2019-10-17 | GSE138997 | GEO

ACSL4 effect on renal ischemia-reperfusion (I/R) injury

Project description:Analysis of acute kidney injury (AKI) with knockdown of ACSL4. Results provide insight into the role of ACSL4 in the regulation of ferroptosis.

2022-02-23 | GSE181842 | GEO

Expression data from livers of female wild-type mice subjected to warm bilateral renal artery ischemia-reperfusion injury (RIR) in comparison to livers of female wild type mice subjected to sham surgery.

Project description:RIR leads to ischemic acute kidney injury (AKI). Women below the age of menopause have a lower incidence of AKI. It is bellieved that estrogens are protective. Many genes were shown to be altered in female wild-type mice subjected to IRI.

2019-10-17 | GSE138996 | GEO

The analysis of differential gene expression after remote ischemic preconditioning of renal ischemia reperfusion injury

Project description:To investigate the mechanism by which ischemic preconditioning (IPC) produces tissue tolerance to renal ischemia reperfusion injury in a pig model 15 female Yorkshire pigs were divided into three groups: 1: no IPC and 90 minutes warm ischemia; 2: remote IPC with an early window followed by 90 min warm ischemia; 3: remote IPC with a late window followed by warm ischemia 24 hrs later. Kidney tissues were obtained after 72 hours.

2016-09-02 | E-GEOD-72646 | biostudies-arrayexpress

Gut-Derived Metabolite Trimethylamine N-Oxide Promotes Inflammation and Fibrosis Following Ischemia/Reperfusion through CCR2-Mediated Macrophage Infiltration

Project description:Inflammation plays a crucial role in the development of acute kidney injury (AKI) and subsequent chronic kidney disease (CKD) following renal ischemia-reperfusion (IR). It has been demonstrated that metabolites from the gut microbiota can trigger inflammatory responses and modulate renal damage induced by IR. However, the exact driving factors and underlying mechanisms of this process remain unclear. Trimethylamine N-oxide (TMAO), a choline metabolite derived from the gut, has been observed to increase in AKI and CKD patients. Our study reveals that glycyrrhizic acid (GA) exacerbates IR-induced AKI and subsequent CKD through TMAO. To delve into the underlying mechanisms, we employed single-cell sequencing to construct a molecular map of kidney cells.

2024-09-09 | GSE244890 | GEO

Tubular-specific ablation of Tiki2 exacerbates inflammation in ischemia/reperfusion-induced acute kidney injury by derepressing Wnt5a/Ror signaling

Project description:Ischemia/reperfusion-induced acute kidney injury (AKI) occurs in several clinical conditions accompanied by inflammation, but the underlying mechanisms remain elusive. The Wnt inhibitor Tiki2 is highly expressed in the kidney with unknown function. Here, we demonstrated that Tiki2 is highly expressed in proximal tubular epithelial cells (PTECs) and is dynamically regulated in AKI. Tubular epithelial cell-specific ablation of Tiki2 aggravated immune cell infiltration and tubular injury in IR-induced AKI. Mechanistically, Tiki2 ablation increased the activity of Wnt5a/Ror signaling, which is activated in PTECs in IR-induced AKI, leading to increased active JNK/ERK signaling and the secretion of chemokines and cytokines to promote the infiltration of immune cells. Furthermore, the increased severity of injury and inflammation caused by Tiki2 ablation could be relieved by knocking down Ror2 in PTECs. Our study reveals the critical roles of Wnt5a/Ror signaling and its negative regulator Tiki2 in IR-induced AKI, which are potential therapeutic targets for treating AKI

2025-04-08 | GSE293486 | GEO

Proteome analysis of membranes from renal ischemia-reperfusion injury mouse models.

Project description:Ischemia-reperfusion injury (IRI) is a well-known model for acute kidney injury (AKI). We applied proteomic analysis to detect membrane proteins from IRI mouse kidneys. The analysis set are composed of negative control (sham operation), samples of 4-hour after IRI, and samples of 8-hour IRI.

2021-09-30 | PXD020708 | JPOST Repository

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