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

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

PROVIDER: PRJNA641095 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12067218.fastq.gz	Fastqsanger.gz
	SRR12067219.fastq.gz	Fastqsanger.gz
	SRR12067220.fastq.gz	Fastqsanger.gz
	SRR12067221.fastq.gz	Fastqsanger.gz
	SRR12067222.fastq.gz	Fastqsanger.gz

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

Project description: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.

2020-06-23 | GSE152972 | GEO

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Project description:Transcriptome analysis was done after warm renal ischemia-reperfusion injury (IRI) in a rat model. Earlier studies have shown a protective effect of prior unilateral nephrectomy (UNx) against IRI in the remaining, contralateral kidney compared to a non-neprectomized control group. We aimed at identifying the underlying molecular mechanisms. We used the Affymetrix Clariom D array (formerly known as RTA 1.0 st.) Array data was processed in the Affymetrix Console Software.

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Gene expression change in Keap1 knockdown (KD) mice in kidneys of ischemia-reperfusion injury (IRI)

Project description:We analyzed differences in IRI kidneys between WT and Keap1 KD mice (= Nrf2-activated mice). To identify Nrf2-target genes or metabolic genes in kidneys, we examined the mRNA expression profile both in normal (uninjured) and IRI kidneys (at day1 after unilateral IRI) from mice We performed microarray analyses using 1) Injured kidneys at day 1 after unilateral IRI, and 2) intact kidneys from mice which did not undergo UIRI. Samples were harvested from Keap1 KD mice and WT mice, n = 2 each,

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Ischemia reperfusion injury (IRI) in organ transplantation and the effects of carbon monoxide treatment

Project description:Ischemia reperfusion injury (IRI) in organ transplantation remains a significant problem with limited alternative therapeutic options. Organs that undergo significant damage during IRI, particularly those enduring long warm ischemia times, undergo significant delayed graft function (DGF) after reperfusion and tend to have greater complications long term with the onset of chronic rejection. The gas molecule carbon monoxide (CO) has emerged as an agent that can suppress IRI in rodent models of solid organ transplantation. Since the use of CO is a potential therapeutic modality in humans, we tested if CO can prevent DGF in a pig model of kidney transplantation Keywords: stress response, treatment response 18 Samples from pig kidneys, two naïve controls, two timepoints, two conditions, 4 replicates

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Gene expression change in Keap1 knockdown (KD) mice in kidneys of ischemia-reperfusion injury (IRI)

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Ischemia reperfusion injury (IRI) in organ transplantation and the effects of carbon monoxide treatment

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miRNome changes in the mouse kidney after unilateral ischemia-reperfusion injury and delayed contralateral nephrectomy

Project description:Comparing the effect of unilateral ischemia-reperfusion injury (IRI) or sham operation (sIRI) with delayed contralateral nephrectomy (Nx) or sham operation (sNx) in mouse kidney. IRI was performed on day 0 and the contralateral kidney was removed on day 7. Mice were sacrificed on day 8. Four animals were selected from the sham IRI-sham Nx and sham IRI-Nx groups and six animals were selected from the IRI-sham Nx and IRI-Nx groups for miRNA microArray analysis on the base of their proinflammatory (TNF-α and IL-6 and CCL2) and immune system-related (Complement component 3) mRNA expression levels.

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Single cell transcriptome analysis of sham and bilateral renal ischemia-reperfusion injury (IRI)

Project description:A rat model of bilateral IRI has been widely used to understand how IRI introduces and progresses the damages on kidney. The aim of this study is to reveal the molecular details of how this bilateral IRI impacts kidney cells. Here, we provide rat single-cell RNA-seq data which is a foundation to understand the IRI related kidney disease. It will support studies to clarify pathophysiology and to develop effective therapy exploiting similar rat renal disease models.

2025-07-18 | GSE208526 | GEO

Gene Expression Changes due to Rat Lung Ischemia-Reperfusion Injury

Project description:Ischemia-reperfusion injury (IRI) is a major cause of morbidity and mortality following conventional lung transplantation and warm ischemia may limit success of transplanting lungs from non-heart-beating donors. We sought to determine alterations in gene expression in rat lung tissue subjected to warm ischemia in vivo followed by reperfusion. Keywords: time course

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Real-time quantitative PCR analysis of Rag1-/- knockout and Rag1-/- Tbx21-/- double knockout mouse liver in a diet- and ischemia-reperfusion injury (IRI)-specific manner.

Project description:Differential gene expression of mouse cytokines and chemokines in Rag1 knockout (Rag1-/- or Rag1-KO) and Rag1-/- Tbx21-/- double knockout (Rag1-Tbet-DKO) was tested in fatty liver ischemic-reperfusion injury (IRI). C57BL/6 mice harboring Rag1-/- or Rag1-/- Tbx21-/- deletions were fed with a normal chow diet (ND, 4.09 kcal/gram,13.4% kJ/fat) or a high-fat diet (HFD, 5.10 kcal/gram, 60% kJ/fat). To induce liver ischemic-reperfusion injury in mice, an atraumatic micro clip was placed across the hepatic hilus, which interrupted the blood supply to the left and median lobes of the liver for 45-minutes of partial warm ischemia time. After 24 hours of liver IRI, the affected left lobe of the liver was harvested and stored in Allprotect Tissue Reagent (Qiagen). We used Qiagen RT² Profiler™ PCR Array for mouse cytokines & chemokines to distinguish immunologically related and diet-specific gene signatures specific to liver IRI in Rag1-KO and Rag1-Tbet-DKO mice.

2022-06-07 | GSE205510 | GEO

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