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Multi-omic map revealed PPARα activation protecting against myocardial ischemia/reperfusion injury by maintaining cardiac metabolic homeostasis.

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

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE240850 | GEO | 2024/08/01

REPOSITORIES: GEO

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Multi-omic map revealed PPARα activation protecting against myocardial ischemia/reperfusion injury by maintaining cardiac metabolic homeostasis [snRNA-seq]

Project description:The rats were subjected to left anterior descending (LAD) coronary artery ligation for 1 hour, 6 hours (MI1h and MI6h) and 24 hours (MI24h) along with Sham controls (Sham), and 1-hour, 6-hour ischemia followed by reperfusion (MI1h/R and MI6h/R, mimicking early time reperfusion (ETR) and late time reperfusion (LTR), respectively) followed by heart tissue collection 24 hours post MI to mimic the MI/R injury in AMI patients.The heart infarct zones (Sham, MI1h/R, MI6h/R and MI24h) were isolated to single-nucleus transcriptome analysis. Collected nuclei for each sample were loaded onto 10X Chrominum platform. We obtained 22,234 cells and 17,003 genes. Five major cell types were identified, which included cardiomyocytes (CMs), endothelial cells (ECs), fibroblasts (FBs), macrophages (MACs) and smooth muscle cells (SMCs).

2024-08-01 | GSE240848 | GEO

Multi-omic map revealed PPARα activation protecting against myocardial ischemia/reperfusion injury by maintaining cardiac metabolic homeostasis [bulk RNA-seq]

2024-08-01 | GSE240847 | GEO

Multi-omic map revealed PPARα activation protecting against myocardial ischemia/reperfusion injury by maintaining cardiac metabolic homeostasis.

Project description:Multi-omic map revealed PPARα activation protecting against myocardial ischemia/reperfusion injury by maintaining cardiac metabolic homeostasis.

| PRJNA1005550 | ENA

Multi-omic map revealed PPARα activation protecting against myocardial ischemia/reperfusion injury by maintaining cardiac metabolic homeostasis [snRNA-seq]

Project description:Multi-omic map revealed PPARα activation protecting against myocardial ischemia/reperfusion injury by maintaining cardiac metabolic homeostasis [snRNA-seq]

| PRJNA1005555 | ENA

Multi-omic map revealed PPARα activation protecting against myocardial ischemia/reperfusion injury by maintaining cardiac metabolic homeostasis [bulk RNA-seq]

Project description:Multi-omic map revealed PPARα activation protecting against myocardial ischemia/reperfusion injury by maintaining cardiac metabolic homeostasis [bulk RNA-seq]

| PRJNA1005554 | ENA

Strontium ions protect hearts against myocardial ischemia/reperfusion injury.

Project description:Timely restoration of blood supply following myocardial infarction is critical to save the infarcted myocardium, while reperfusion would cause additional damage. Strontium ions have been shown to promote angiogenesis, but it is unknown whether they can save the damaged myocardium. We report that myocardial ischemia/reperfusion (I/R)-induced functional deterioration and scar formation were notably attenuated by injection of strontium ion-containing composite hydrogels into murine infarcted myocardium at 20 minutes of reperfusion following 60 minutes of ischemia. These beneficial effects were accompanied by reduced cardiomyocyte apoptosis and increased angiogenesis. The effects of strontium ions were further confirmed by the enhanced viability of cardiomyocytes and stimulated angiogenesis in vitro. These findings are the first to reveal the cardioprotective effects of strontium ions against I/R injury, which may provide a new therapeutic approach to ischemic heart disease at a lower cost, with higher stability, and with potentially greater safety.

| S-EPMC7810382 | biostudies-literature

Project description:BackgroundCathelicidins are a major group of natural antimicrobial peptides which play essential roles in regulating host defense and immunity. In addition to the antimicrobial and immunomodulatory activities, recent studies have reported the involvement of cathelicidins in cardiovascular diseases by regulating inflammatory response and microvascular dysfunction. However, the role of cathelicidins in myocardial apoptosis upon cardiac ischemia/reperfusion (I/R) injury remains largely unknown.MethodsCRAMP (cathelicidin-related antimicrobial peptide) levels were measured in the heart and serum from I/R mice and in neonatal mouse cardiomyocytes treated with oxygen glucose deprivation/reperfusion (OGDR). Human serum cathelicidin antimicrobial peptide (LL-37) levels were measured in myocardial infarction (MI) patients. The role of CRAMP in myocardial apoptosis upon I/R injury was investigated in mice injected with the CRAMP peptide and in CRAMP knockout (KO) mice, as well as in OGDR-treated cardiomyocytes.ResultsWe observed reduced CRAMP level in both heart and serum samples from I/R mice and in OGDR-treated cardiomyocytes, as well as reduced LL-37 level in MI patients. Knockdown of CRAMP enhanced cardiomyocyte apoptosis, and CRAMP KO mice displayed increased infarct size and myocardial apoptosis. In contrast, the CRAMP peptide reduced cardiomyocyte apoptosis and I/R injury. The CRAMP peptide inhibited cardiomyocyte apoptosis by activation of Akt and ERK1/2 and phosphorylation and nuclear export of FoxO3a. c-Jun was identified as a negative regulator of the CRAMP gene. Moreover, lower level of serum LL-37/neutrophil ratio was associated with readmission and/or death in MI patients during 1-year follow-up.ConclusionsCRAMP protects against cardiomyocyte apoptosis and cardiac I/R injury via activation of Akt and ERK and phosphorylation and nuclear export of FoxO3a. Increasing LL-37 might be a novel therapy for cardiac ischemic injury.

| S-EPMC6381635 | biostudies-literature

PIAS1 protects against myocardial ischemia-reperfusion injury by stimulating PPARγ SUMOylation.

Project description:BackgroundMyocardial ischemia-reperfusion injury (IRI) has become one of the most serious complications after reperfusion therapy in patients with acute myocardial infarction. Small ubiquitin-like modification (SUMOylation) is a reversible process, including SUMO E1-, E2-, and E3-mediated SUMOylation and SUMO-specific protease-mediated deSUMOylation, with the latter having been shown to play a vital role in myocardial IRI previously. However, little is known about the function and regulation of SUMO E3 ligases in myocardial IRI.ResultsIn this study, we found dramatically decreased expression of PIAS1 after ischemia/reperfusion (I/R) in mouse myocardium and H9C2 cells. PIAS1 deficiency aggravated apoptosis and inflammation of cardiomyocytes via activating the NF-κB pathway after I/R. Mechanistically, we identified PIAS1 as a specific E3 ligase for PPARγ SUMOylation. Moreover, H9C2 cells treated with hypoxia/reoxygenation (H/R) displayed reduced PPARγ SUMOylation as a result of down-regulated PIAS1, and act an anti-apoptotic and anti-inflammatory function through repressing NF-κB activity. Finally, overexpression of PIAS1 in H9C2 cells could remarkably ameliorate I/R injury.ConclusionsCollectively, our findings demonstrate the crucial role of PIAS1-mediated PPARγ SUMOylation in protecting against myocardial IRI.

| S-EPMC6233564 | biostudies-literature

Intrathecal Administration of Nanoclusters for Protecting Neurons against Oxidative Stress in Cerebral Ischemia/Reperfusion Injury.

Project description:Oxidative stress is one of the important mechanisms in cerebral ischemia/reperfusion (I/R) injury. Antioxidants with high brain accumulation are highly desired to help prevent cerebral I/R injury. Herein, intrathecal injection of polyoxometalate (POM) nanoclusters as nano-antioxidants with preferential brain uptake were applied for neuronal protection in cerebral I/R injury. Using powerful positron emission tomography imaging, the uptake of nano-antioxidants in the brain was non-invasively and real-timely monitored. Our results demonstrated that POM nanoclusters rapidly reached the ischemic penumbra after intrathecal injection and effectively scavenged reactive oxygen species (ROS) for inhibiting oxidative stress. The infarct size was reduced, and neurological function was restored in cerebral I/R injury rat models. As a proof-of-concept, the intrathecal injection of nano-antioxidants is an excellent therapeutic strategy to ameliorate cerebral I/R injury.

| S-EPMC6881527 | biostudies-literature

Spatial multi-omic map of human myocardial infarction.

Project description:Myocardial infarction is a leading cause of death worldwide1. Although advances have been made in acute treatment, an incomplete understanding of remodelling processes has limited the effectiveness of therapies to reduce late-stage mortality2. Here we generate an integrative high-resolution map of human cardiac remodelling after myocardial infarction using single-cell gene expression, chromatin accessibility and spatial transcriptomic profiling of multiple physiological zones at distinct time points in myocardium from patients with myocardial infarction and controls. Multi-modal data integration enabled us to evaluate cardiac cell-type compositions at increased resolution, yielding insights into changes of the cardiac transcriptome and epigenome through the identification of distinct tissue structures of injury, repair and remodelling. We identified and validated disease-specific cardiac cell states of major cell types and analysed them in their spatial context, evaluating their dependency on other cell types. Our data elucidate the molecular principles of human myocardial tissue organization, recapitulating a gradual cardiomyocyte and myeloid continuum following ischaemic injury. In sum, our study provides an integrative molecular map of human myocardial infarction, represents an essential reference for the field and paves the way for advanced mechanistic and therapeutic studies of cardiac disease.

| S-EPMC9364862 | biostudies-literature

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