Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Blockade of the G-CSFR or C5 in a murine model of unilateral warm renal ischemia-reperfusion injury (IRI).

ABSTRACT: Purpose: Understand gene transcriptional changes in kidney cell populations after ischemia-reperfusion injury and after treatment with either a neutralizing mAb to the G-CSFR or a neutralizing mAb to C5.

ORGANISM(S): Mus musculus

PROVIDER: GSE152972 | GEO | 2020/06/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Blockade of the G-CSFR or C5 in a murine model of unilateral warm renal ischemia-reperfusion injury (IRI).

Project description:Blockade of the G-CSFR or C5 in a murine model of unilateral warm renal ischemia-reperfusion injury (IRI).

| PRJNA641095 | ENA

Billgrantia sp. C5 strain:C5 | isolate:C5

Project description:Billgrantia sp. C5 strain:C5 | isolate:C5 Genome sequencing

| PRJNA1273590 | ENA

G-CSF receptor targeting in inflammatory arthritis

Project description:G-CSF is a hemopoietic growth factor that has a role in steady state granulopoiesis, as well as in mature neutrophil activation and function. We developed a neutralizing monoclonal antibody to the murine G-CSF receptor (G-CSFR), which antagonizes binding of murine G-CSF and inhibits G-CSFR signalling. Anti-G-CSFR rapidly halts the progression of established disease in collagen antibody-induced arthritis (CAbIA). Neutrophil accumulation in joints is inhibited, without rendering animals neutropenic, suggesting an effect on homing to inflammatory sites. Neutrophils in the blood and arthritic joints of anti-G-CSFR treated mice show alterations in cell adhesion receptors, while anti-G-CSFR suppresses local production of proinflammatory cytokines and chemokines known to drive tissue damage. Our aim in this study was to use differential gene expression analysis of joint and blood neutrophils to more thoroughly understand the effect of G-CSFR blockade on the inflammatory response following anti-G-CSFR therapy in CAbIA. C57BL/6 mice with collagen antibody-induced arthritis were injected intra-peritoneally at day 5 with 50 Î¼g anti-G-CSFR (n = 20 mice) or control mAb (n = 10 mice). At day 7, neutrophils (CD45+ CD11bhi Ly6G+) were sorted (BD FACSAria) from pooled digests of the knee tissues, or peripheral blood, and the RNA was extracted from 3 such experiments, giving a total of 12 samples.

2016-01-19 | E-GEOD-76966 | biostudies-arrayexpress

Bipolaris maydis C5 strain:C5

Project description:Bipolaris maydis C5 strain:C5 Transcriptome or Gene expression

| PRJNA43339 | ENA

Alkalibacillus haloalkaliphilus C5 strain:C5

Project description:Alkalibacillus haloalkaliphilus C5 strain:C5 Genome sequencing and assembly

| PRJNA167217 | ENA

Sulfurimonas sp. C5 strain:C5

Project description:Sulfurimonas sp. C5 strain:C5 Genome sequencing and assembly

| PRJNA949113 | ENA

Neu3 Sialidase Activates the RISK Cardioprotective Signaling Pathway during Ischemia and Reperfusion Injury (IRI).

Project description:Coronary reperfusion strategies are life-saving approaches to restore blood flow to cardiac tissue after acute myocardial infarction (AMI). However, the sudden restoration of normal blood flow leads to ischemia and reperfusion injury (IRI), which results in cardiomyoblast death, irreversible tissue degeneration, and heart failure. The molecular mechanism of IRI is not fully understood, and there are no effective cardioprotective strategies to prevent it. In this study, we show that activation of sialidase-3, a glycohydrolytic enzyme that cleaves sialic acid residues from glycoconjugates, is cardioprotective by triggering RISK pro-survival signaling pathways. We found that overexpression of Neu3 significantly increased cardiomyoblast resistance to IRI through activation of HIF-1α and Akt/Erk signaling pathways. This raises the possibility of using Sialidase-3 activation as a cardioprotective reperfusion strategy after myocardial infarction.

| S-EPMC9181429 | biostudies-literature

Bipolaris maydis C5 strain:C5

Project description:Cochliobolus heterostrophus C5 genome project

| PRJNA42739 | ENA

Gene expression in kidney cells after unilateral ischemia-reperfusion

Project description:To determine changes in gene expression due to ischemia-reperfusion AKI in different intra-renal cell populations

2024-04-17 | GSE263369 | GEO

Melatonin and Glycine Reduce Uterus Ischemia/Reperfusion Injury in a Rat Model of Warm Ischemia.

Project description:Ischemia/reperfusion injury (IRI) remains a significant problem to be solved in uterus transplantation (UTx). Melatonin and glycine have been shown to possess direct cytoprotective activities, mainly due to their antioxidative and anti-inflammatory properties. The aim of this study was to investigate the protective effects of melatonin and glycine and their combination on IRI in a rat model of warm ischemia. In this study, Sprague-Dawley rats were assigned to eight groups, including sham and IRI (n = 80). Melatonin and glycine alone or their combination were administered prior to 1 h of uterus ischemia followed by 1 h of reperfusion. Melatonin (50 mg/kg) was administered via gavage 2 h before IRI and glycine in an enriched diet for 5 days prior to intervention. Uterus IRI was estimated by histology, including immunohistochemistry, and biochemical tissue analyses. Histology revealed that uterus IRI was significantly attenuated by pretreatment with melatonin (p = 0.019) and glycine (p = 0.044) alone as well as their combination (p = 0.003). Uterus IRI led to increased myeloperoxidase expression, which was significantly reduced by melatonin (p = 0.004), glycine (p < 0.001) or their combination (p < 0.001). The decline in superoxide dismutase activity was significantly reduced in the melatonin (p = 0.027), glycine (p = 0.038) and combined treatment groups (p = 0.015) when compared to the IRI control group. In conclusion, melatonin, glycine and their combination significantly reduced oxidative stress-induced cell damage after IRI in a small animal warm ischemia model, and, therefore, clinical studies are required to evaluate the protective effects of these well-characterized substances in uterus IRI.

| S-EPMC8394613 | biostudies-literature

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