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Metformin preconditioning protects against myocardial stunning and preserves mitochondrial dynamics and protein translation in a mouse model of cardiac arrest

ABSTRACT: Metformin preconditioning protects against myocardial stunning and preserves mitochondrial dynamics and protein translation in a mouse model of cardiac arrest

PROVIDER: PRJNA736430 | ENA |

REPOSITORIES: ENA

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Metformin preconditioning protects against myocardial stunning and preserves mitochondrial dynamics and protein translation in a mouse model of cardiac arrest

Project description:We compare microarray data from homogenized left ventricles of the heart at 24 hours after sham surgey vs 8-min potassium chloride induced sudden cardiac arrest and resuscitation

2021-08-01 | GSE176494 | GEO

Metformin preconditioning protects against myocardial stunning and preserves protein translation in a mouse model of cardiac arrest.

Project description:Cardiac arrest (CA) causes high mortality due to multi-system organ damage attributable to ischemia-reperfusion injury. Recent work in our group found that among diabetic patients who experienced cardiac arrest, those taking metformin had less evidence of cardiac and renal damage after cardiac arrest when compared to those not taking metformin. Based on these observations, we hypothesized that metformin's protective effects in the heart were mediated by AMPK signaling, and that AMPK signaling could be targeted as a therapeutic strategy following resuscitation from CA. The current study investigates metformin interventions on cardiac and renal outcomes in a non-diabetic CA mouse model. We found that two weeks of metformin pretreatment protects against reduced ejection fraction and reduces kidney ischemia-reperfusion injury at 24 h post-arrest. This cardiac and renal protection depends on AMPK signaling, as demonstrated by outcomes in mice pretreated with the AMPK activator AICAR or metformin plus the AMPK inhibitor compound C. At this 24-h time point, heart gene expression analysis showed that metformin pretreatment caused changes supporting autophagy, antioxidant response, and protein translation. Further investigation found associated improvements in mitochondrial structure and markers of autophagy. Notably, Western analysis indicated that protein synthesis was preserved in arrest hearts of animals pretreated with metformin. The AMPK activation-mediated preservation of protein synthesis was also observed in a hypoxia/reoxygenation cell culture model. Despite the positive impacts of pretreatment in vivo and in vitro, metformin did not preserve ejection fraction when deployed at resuscitation. Taken together, we propose that metformin's in vivo cardiac preservation occurs through AMPK activation, requires adaptation before arrest, and is associated with preserved protein translation.

| S-EPMC10327679 | biostudies-literature

Blast preconditioning protects retinal ganglion cells and reveals targets for prevention of neurodegeneration following blast-mediated TBI

Project description:Purpose: The purpose of this study was to examine the effect blast preconditioning on the structure and function of retinal ganglion cells (RGC), and to identify molecular pathways that contribute to RGC loss. Methods: To examine the effect of blast-preconditioning three groups of mice were analyzed, including those 1) subjected to sham injury followed by one single 20 PSI injury one week later, 2) mice exposed to two low intensity preconditioning blast exposures separated by one week (5 PSI, 5 PSI) and 3) mice exposed to a preconditioning injury (5 PSI) followed by a single 20 PSI blast exposure one week later. RNAseq analysis was used to identify transcriptional changes between groups. Conclusions: Preconditioning protects RGC from blast injury. Protective effects appear to involve changes in kynurenine-3-monooxygenase activity, whose inhibition is also protective.

2019-09-24 | GSE133940 | GEO

Genomics of preconditioning

Project description:Isolated perfused rat hearts exposed to isoflurane or ischemic preconditioning, a subgroup followed by 40 minutes of ischemia and 3 hours of reperfusion. Exact protocol available from the authors. Keywords = preconditioning Keywords = anesthetics Keywords = ischemia/reperfusion Keywords: other

2004-07-30 | GSE1616 | GEO

Protective effect of remote ischemic preconditioning combined with sevoflurane posttreatment on myocardial injury during laparoscopic radical resection of colorectal cancer

Project description:Interventions: total intravenous anesthesia:Propofol anesthesia;Sevoflurane posttreatment:Sevoflurane anesthesia;Propofol combined with sevoflurane anesthesia:Propofol combined with sevoflurane anesthesia;RIPC and propofol anesthesia:Remote ischemic preconditioning and propofol anesthesia;RIPC and sevoflurane posttreatment:Remote ischemic preconditioning and sevoflurane anesthesia;RIPC and propofol combined with sevoflurane anesthesia:Remote ischemic preconditioning and propofol combined with sevoflurane anesthesia Primary outcome(s): blood pressure;heart rate;SPO2%;Blood gas analysis;Central venous pressure;H-FABP;cTnI;TNF-a;IL-8 Study Design: Parallel

| 2703482 | ecrin-mdr-crc

Preconditioning Biochar-Fungal analyses

Project description:Preconditioning Biochar-Fungal analyses

| PRJNA415278 | ENA

RNAseq of C. elegans cultured on metformin sensitive and resistant E. coli strains with and without 50mM metformin treatment.

Project description:Metformin is the therapy of choice for treating type 2 diabetes and is currently repurposed for a wide range of diseases including aging. Recent evidence implicates the gut microbiota as a site of metformin action. Combining two tractable genetic models, the bacterium E. coli and the nematode C. elegans, we performed C. elegans RNAseq to investigate the role of the metformin sensitive OP50 and metformin resistant OP50-MR E. coli microbiota in the drug effects on the host. Our data suggest an evolutionarily conserved bacterial mediation of metformin effects on host lipid metabolism and lifespan.

2019-07-13 | E-MTAB-7272 | biostudies-arrayexpress

Mitochondria preconditioning delays aging and associated diseases in C. elegans impacting on key ferroptosis players

Project description:Excessive iron accumulation or deficiency have detrimental consequences across species, leading to a variety of pathologies in humans. In the nematode Caenorhabditis elegans severe iron as well as oxygen deprivation induce developmental arrest. Instead, hypoxia preconditioning protects against severe hypoxia-induced neuromuscular damage and sub-lethal levels of iron depletion extend lifespan in C. elegans. The positive health outcomes of applying hypoxia preconditioning are obvious but have low feasible application. Here, we thus assessed the potential beneficial effects of genetic and chemical interventions acting via mild iron instead of oxygen depletion. We show that limiting iron availability through frataxin silencing or the iron chelator bipyridine, similar to hypoxia preconditioning, protect against hypoxia-, age- and proteotoxicityinduced neuromuscular deficits. Mechanistically, our data suggest that the beneficial effects elicited by frataxin silencing are at least in part mediated by counteracting ferroptosis, a form of non-apoptotic cell death specifically mediated by iron-induced lipid peroxidation. These is achieved by impacting on different key players of the ferroptosis machinery and likely via novel, gpx-independent redox systems. We thus point to ferroptosis inhibition as a novel strategy to promote healthy aging.

2023-04-17 | PXD040724 | Pride

Effect of Gilteritinib, Metformin and Combination treatments on gene expression in MOLM13-RES cells

Project description:Here, we report that Metformin shows a striking synergistic effect with Gilteritinib in suppressing cell proliferation and promoting apoptosis and cell cycle arrest in multiple FLT3-ITD AML cell lines, including FLT3 TKI-resistant MOLM13 cells. Mechanistically, the combinational treatment synergistically suppresses Polo-like kinase 1 (PLK1) expression and phosphorylation of FLT3/STAT5/ERK/mTOR in MOLM13-RES cells. Intriguingly, our retrospective clinical analysis has unveiled a significant correlation between Metformin intake and improved survival rates among FLT3-ITD AML patients. Collectively, the cotreatment of Metformin and Gilteritinib shows robustly enhanced therapeutic efficacy in treating FLT3-mutated AML by synergistically suppressing PLK1 expression and phosphorylation of FLT3/STAT5/ERK/mTOR.

2024-06-14 | GSE244855 | GEO

A Drosophila screen identifies a role for histone methylation in ER stress preconditioning

Project description:Stress preconditioning occurs when transient, sublethal stress events impact an organism's ability to counter future stresses. Although preconditioning effects are often noted in the literature, very little is known about the underlying mechanisms. To model preconditioning, we exposed a panel of genetically diverse Drosophila melanogaster to a sublethal heat shock and measured how well the flies survived exposure to endoplasmic reticulum (ER) stress. To identify genes with expression patterns predictive of preconditioning outcomes, we focused on the 10 DGRP strains at the extreme ends of our preconditioning screen. We compared the beneficial strains (RAL69, RAL93, RAL359, RAL387, RAL409) to the detrimental (RAL195, RAL304, RAL335, RAL737, RAL819) with and without heat shock (our preconditioning stress).

2023-04-25 | GSE226958 | GEO

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