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Transcriptional analysis on ischemia-reperfusion injury of mouse normal or steatotic livers

ABSTRACT: More and more steatotic livers undergo resection or transplantation but they exhibit higher susceptibility to ischemia-reperfusion injury (IRI), which results in increased perioperative complication morbidity and mortality. To investigate the underlying mechanisms, we conducted RNA-seq with liver samples derived from mice that were fed either high-fat-diet (HFD) or normal diet (ND) and experienced either IRI or sham operation.

ORGANISM(S): Mus musculus

PROVIDER: GSE279693 | GEO | 2025/12/04

REPOSITORIES: GEO

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ZBP1-mediated apoptosis and inflammation exacerbate steatotic liver ischemia/reperfusion injury

Project description:Abstract Background & Aims: In liver transplantation, steatotic donor livers are rapidly increasing but are more susceptible to ischemia-reperfusion (I/R) injury. This study aimed to investigate the underlying mechanisms and identify therapeutic targets. Methods: Cell death markers were determined in donor livers and animal models. Casp8f/f;Alb-Cre, Ripk1D138N/D138N, Tnf-/-, Ripk3-/-, Trif-/-, Zbp1-/- mice were fed high fat diet or choline-deficient high fat diet to induce steatotic livers and were then subjected to I/R injury to investigate the mechanisms of cell death and inflammation. Primary mouse or human hepatocytes were isolated and subjected to hypoxia-reoxygenation challenge to further elucidate the regulation mechanisms. Results: Apoptosis- and inflammation-induced injury was exacerbated in I/R process of steatotic livers, with inflammation-induced injury playing a more predominant role. In both normal and steatotic livers, caspase-8 ablation mitigated I/R injury by reducing apoptosis but not inflammation while RIPK1 kinase inhibition more effectively protected against I/R injury by alleviating both apoptosis and inflammation. Z-DNA binding protein 1 (ZBP1) but not TNF-α deficiency inhibited RIPK1 activation and protected against I/R injury in steatotic livers but not normal livers. In steatotic livers, overmuch palmitic acid triggered ZBP1 transcription through activating JNK pathway. During liver transplantation, excessive reactive oxygen species were generated during I/R injury and triggered ZBP1 oligomerization, which led to the kinase activation of RIPK1 and the subsequent aggravation of apoptosis- and inflammation-induced injury. Conclusions: ZBP1-mediated apoptosis and inflammation exacerbate steatotic liver I/R injury, which could be leveraged to protect steatotic donor livers in transplantation.

2024-06-01 | GSE254747 | 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

Murine Kidney cells: Control versus Ischemia reperfusion injury

Project description:miRNA profiling of kidney tissue from C57BL/6 mice that received a 30 minute ischemic injury compared with control kidney tissue from mice that received sham operation only. Two condition experiment - sham and ishemic injury (IRI). Eight time points were measured using pooled samples from three mice.

2011-07-31 | E-GEOD-29495 | biostudies-arrayexpress

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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Acute kidney injury following fatty liver ischemia-reperfusion injury: indirect protection by hepatic ferroptosis inhibition

Project description:To understand the roles of ferroptosis in subsequent acute kidney injury (AKI) following hepatic ischemia-reperfusion injury (hIRI) in steatosis livers. The hIRI was induced in mice fed either a high-fat, high-sucrose diet (HFD) or a normal diet (ND) to mimic the AKI commonly observed clinically after fatty liver transplantation. RNA sequencing was conducted to investigate the underlying mechanisms. We found that apoptosis and inflammation are the prominent kidney injury mechanisms following fatty liver IRI. Although ferroptosis may not be directly involved in the renal injury, anti-ferroptosis intervention mitigates AKI, supporting the concept that ferroptosis-mediated liver injury may serve as the primary upstream trigger in this context.

2025-11-21 | GSE309904 | GEO

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

Protective effect of ischemic postconditioning on ischemia reperfusion injury in steatotic rat livers.

Project description: Not available

| S-EPMC8422122 | biostudies-literature

Transcriptional analysis on ischemia-reperfusion injury of mouse normal or steatotic livers

Project description:Transcriptional analysis on ischemia-reperfusion injury of mouse normal or steatotic livers

| PRJNA1178563 | ENA

Transcriptional analysis on ischemia-reperfusion injury of mouse normal or steatotic livers

Project description:Transcriptional analysis on ischemia-reperfusion injury of mouse normal or steatotic livers

| PRJNA1174092 | ENA

Proteomic Analysis of Kidney Tissues Following Ischemia-Reperfusion Injury in Male Mice

Project description:Renal ischemia-reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI) and presents significant challenges during kidney transplantation. Due to the detrimental effects of IRI on kidney function and the lack of effective intervention strategies, we conduct a multi-omics study on surgically induced mouse IRI, revealing a modulatory role for the metabolite S-adenosylmethionine (SAM) in AKI development. Our metabolic analysis of clinical samples establishes a link between various AKI conditions and marked elevations in serum SAM, underlying its potential as a biomarker for diagnosis. Furthermore, we find that short-term dietary methionine deprivation, which reduces circulating methionine and kidney SAM levels, effectively enhances renal resilience against IRI. In vivo isotopic tracing demonstrates that this diet preconditions kidney metabolic programs, enhancing glucose and fatty acid oxidation in preparation for IRI. Particularly, the activation of pyruvate dehydrogenase, which produces acetyl-CoA to fuel the tricarboxylic acid (TCA) cycle, highlights an energy-efficient strategy of glucose metabolism that is essential for the protective effects of dietary methionine deprivation.

2025-12-06 | PXD058530 | Pride

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