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Hepatic response to ischemia and reperfusion: young and adult mice

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE10657 | GEO | 2008/03/01

SECONDARY ACCESSION(S): PRJNA107623

REPOSITORIES: GEO

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Hepatic response to ischemia and reperfusion: young and adult mice

Project description:This SuperSeries is composed of the following subset Series: GSE10652: Divergent genome expression profiles during hepatic ischemia in young and adult mice GSE10654: Age-dependent gene expression profiles after hepatic ischemia/reperfusion in mice Keywords: SuperSeries Refer to individual Series

2010-05-26 | E-GEOD-10657 | biostudies-arrayexpress

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ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury

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Diminazene aceturate attenuates hepatic ischemia/reperfusion injury in mice.

Project description:Hepatic ischemia/reperfusion (I/R) injury is one of the leading causes of mortality following partial hepatectomy, liver transplantation, hypovolemic shock and trauma; however, effective therapeutic targets for the treatment of hepatic I/R injury are lacking. Recent studies have shown that diminazene aceturate (DIZE) has protective effects against inflammation, oxidative stress and cell death, which are the main pathogenetic mechanisms associated with hepatic I/R injury. However, the mechanistic effects DIZE exerts on hepatic I/R remain unknown. C57BL/6 male mice were pretreated with either 15 mg/kg DIZE or vehicle control (saline) and subjected to partial liver ischemia for 60 min. One day after induction of hepatic I/R, liver damage, inflammatory responses, oxidative stress and apoptosis were analyzed. By evaluating plasma alanine aminotransferase levels and histology, we found that DIZE treatment attenuated liver failure and was associated with a reduction in histologically-apparent liver damage. We also found that DIZE-treated mice had milder inflammatory responses, less reactive oxidative damage and less apoptosis following hepatic I/R compared to vehicle-treated mice. Taken together, our study demonstrates that DIZE protects against ischemic liver injury by attenuating inflammation and oxidative damage and may be a potential therapeutic agent for the prevention and treatment of ischemic liver failure.

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Heart expression data after short ischemia/reperfusion in WT, Reverb alpha KO and Reverb alpha antagonist-treated mice

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Divergent genome expression profiles during hepatic ischemia in young and adult mice

Project description:Experimental Design: 1. The goal of the experiment: Age-Related Genome Expression Profiles During Hepatic Ischemia 2. Brief description of the experiment: Hepatic ischemia/reperfusion (I/R) injury is a complication of liver surgery, transplantation and shock and differs with age. In the present study, we sought to determine if the age-dependent response to I/R injury was related to differential gene expression during the ischemic period. Total RNA of young (4-5 weeks) and adult (12-14 months) mice undergoing sham surgery or partial hepatic ischemia for 30, 60, or 90 minutes was analyzed by Affymetrix microarray. Gene expression was filtered based on a change in expression of 1.5-fold relative to respective controls and then analyzed by ANOVA. Significant differences in gene expression were observed between age groups. In young mice, 169 genes were down-regulated, whereas adult mice had 1167 genes down-regulated. Of these, only 28 genes were down-regulated in both young and adult mice. Far fewer genes had increased expression during ischemia. Sixty genes in young mice and 51 genes in adult mice were up-regulated. Of those, none were up-regulated in both young and adult mice. There were no distinct functional patterns of gene regulation in either age group. The data demonstrate significant and widespread changes in hepatic gene expression during the ischemic period that may be important to the age-dependent response to I/R injury. Keywords: treated vs non treated 2 age groups of 12 young and 12 adult mice that underwent either 30, 60 or 90 minutes of partial ischemia (n=3) or sham operation (n=3) We used microarray to uncover the genomic response during different time points of ischemia

2010-05-26 | E-GEOD-10652 | biostudies-arrayexpress

Monoacylglycerol Acyltransferase 1 Knockdown Exacerbates Hepatic Ischemia/Reperfusion Injury in Mice With Hepatic Steatosis.

Project description:Nonalcoholic fatty liver disease (NAFLD) is becoming the most common indication for liver transplantation. The growing prevalence of NAFLD not only increases the demand for liver transplantation, but it also limits the supply of available organs because steatosis predisposes grafts to ischemia/reperfusion injury (IRI) and many steatotic grafts are discarded. We have shown that monoacylglycerol acyltransferase (MGAT) 1, an enzyme that converts monoacylglycerol to diacylglycerol, is highly induced in animal models and patients with NAFLD and is an important mediator in NAFLD-related insulin resistance. Herein, we sought to determine whether Mogat1 (the gene encoding MGAT1) knockdown in mice with hepatic steatosis would reduce liver injury and improve liver regeneration following experimental IRI. Antisense oligonucleotides (ASO) were used to knockdown the expression of Mogat1 in a mouse model of NAFLD. Mice then underwent surgery to induce IRI. We found that Mogat1 knockdown reduced hepatic triacylglycerol accumulation, but it unexpectedly exacerbated liver injury and mortality following experimental ischemia/reperfusion surgery in mice on a high-fat diet. The increased liver injury was associated with robust effects on the hepatic transcriptome following IRI including enhanced expression of proinflammatory cytokines and chemokines and suppression of enzymes involved in intermediary metabolism. These transcriptional changes were accompanied by increased signs of oxidative stress and an impaired regenerative response. We have shown that Mogat1 knockdown in a mouse model of NAFLD exacerbates IRI and inflammation and prolongs injury resolution, suggesting that Mogat1 may be necessary for liver regeneration following IRI and that targeting this metabolic enzyme will not be an effective treatment to reduce steatosis-associated graft dysfunction or failure.

| S-EPMC7785593 | biostudies-literature

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