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Macrophage-produced VEGFC is induced by efferocytosis to resolve inflammation and improve ventricular function after myocardial infarction

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

ORGANISM(S): Mus musculus

PROVIDER: GSE196867 | GEO | 2022/03/31

REPOSITORIES: GEO

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Macrophage-produced VEGFC is induced by efferocytosis to resolve inflammation and improve ventricular function after myocardial infarction (RNA-Seq)

Project description:Recent reports have suggested a protective role for vascular endothelial growth factor C (VEGFC) during acute cardiac lymphangiogenesis post MI. Glinton et al. report that defective efferocytosis by macrophages after experimental MI leads to a reduction in cardiac lymphangiogenesis and Vegfc expression.

2022-03-31 | GSE196866 | GEO

Macrophage-produced VEGFC is induced by efferocytosis to resolve inflammation and improve ventricular function after myocardial infarction (ChIP-Seq)

2022-03-31 | GSE196865 | GEO

Macrophage-produced VEGFC is induced by efferocytosis to resolve inflammation and improve ventricular function after myocardial infarction

Project description:Macrophage-produced VEGFC is induced by efferocytosis to resolve inflammation and improve ventricular function after myocardial infarction

| PRJNA807628 | ENA

Macrophage-produced VEGFC is induced by efferocytosis to resolve inflammation and improve ventricular function after myocardial infarction (RNA-Seq)

Project description:Macrophage-produced VEGFC is induced by efferocytosis to resolve inflammation and improve ventricular function after myocardial infarction (RNA-Seq)

| PRJNA807633 | ENA

Macrophage-produced VEGFC is induced by efferocytosis to resolve inflammation and improve ventricular function after myocardial infarction (ChIP-Seq)

Project description:Macrophage-produced VEGFC is induced by efferocytosis to resolve inflammation and improve ventricular function after myocardial infarction (ChIP-Seq)

| PRJNA807634 | ENA

Engineered neutrophil apoptotic bodies ameliorate myocardial infarction by promoting macrophage efferocytosis and inflammation resolution

Project description:Inflammatory response plays a critical role in myocardial infarction (MI) repair. The neutrophil apoptosis and subsequent macrophage ingestion can result in inflammation resolution and initiate regeneration, while the therapeutic strategy that simulates and enhances this natural process has not been established. Here, we constructed engineered neutrophil apoptotic bodies (eNABs) to simulate natural neutrophil apoptosis, which regulated inflammation response and enhanced MI repair. The eNABs were fabricated by combining natural neutrophil apoptotic body membrane which has excellent inflammation-tropism and immunoregulatory properties, and mesoporous silica nanoparticles loaded with hexyl 5-aminolevulinate hydrochloride (HAL). The eNABs actively targeted to macrophages and the encapsulated HAL simultaneously initiated the biosynthesis pathway of heme to produce anti-inflammatory bilirubin after intracellular release, thereby further enhancing the anti-inflammation effects. In in vivo studies, the eNABs efficiently modulated inflammation responses in the infarcted region to ameliorate cardiac function. This study demonstrates an effective biomimetic construction strategy to regulate macrophage functions for MI repair. Graphical abstract Image 1 Highlights • Construction of engineered neutrophil apoptotic bodies to simulate natural neutrophil apoptosis.• Engineered neutrophil apoptotic bodies with excellent inflammation-tropism and macrophage-specific targeting capacity.• Engineered neutrophil apoptotic bodies enhance macrophage efferocytosis and reprogramming for inflammation resolution.• Engineered neutrophil apoptotic bodies ameliorate myocardial infarction and promote cardiac tissue regeneration after MI.

| S-EPMC8586716 | biostudies-literature

PCSK9 Modulates Macrophage Polarization-Mediated Ventricular Remodeling after Myocardial Infarction.

Project description:Background and aimsAn increasing number of high-risk patients with coronary heart disease (similar to acute myocardial infarction (AMI)) are using PCSK9 inhibitors. However, whether PCSK9 affects myocardial repair and the molecular mechanism of PCSK9 modulation of immune inflammation after AMI are not known. The present research investigated the role of PCSK9 in the immunomodulation of macrophages after AMI and provided evidence for the clinical application of PCSK9 inhibitors after AMI to improve cardiac repair.Methods and resultsWild-type C57BL6/J (WT) and PCSK9-/- mouse hearts were subjected to left anterior descending (LAD) coronary artery occlusion to establish an AMI model. Correlation analysis showed that higher PCSK9 expression indicated worse cardiac function after AMI, and PCSK9 knockout reduced infarct size, improved cardiac function, and attenuated inflammatory cell infiltration compared to WT mice. Notably, the curative effects of PCSK9 inhibition were abolished after the systemic depletion of macrophages using clodronate liposomes. PCSK9 showed a regulatory effect on macrophage polarization in vivo and in vitro. Our studies also revealed that activation of the TLR4/MyD88/NF-κB axis was a possible mechanism of PCSK9 regulation of macrophage polarization.ConclusionOur data suggested that PCSK9 modulated macrophage polarization-mediated ventricular remodeling after myocardial infarction.

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Trem2 Macrophage Promote Cardiac Repair in Myocardial Infarction via Efferocytosis and Carbohydrate Metabolism

Project description:We want to find that the TREM2 mechanism on the Macrophages in the myocardial infarction

2022-11-15 | GSE218002 | GEO

Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction.

Project description:Galectin-1 (Gal-1), an evolutionarily conserved ?-galactoside-binding lectin, plays essential roles in the control of inflammation and neovascularization. Although identified as a major component of the contractile apparatus of cardiomyocytes, the potential role of Gal-1 in modulating heart pathophysiology is uncertain. Here, we aimed to characterize Gal-1 expression and function in the infarcted heart. Expression of Gal-1 was substantially increased in the mouse heart 7 days after acute myocardial infarction (AMI) and in hearts from patients with end-stage chronic heart failure. This lectin was localized mainly in cardiomyocytes and inflammatory infiltrates in peri-infarct areas, but not in remote areas. Both simulated hypoxia and proinflammatory cytokines selectively up-regulated Gal-1 expression in mouse cardiomyocytes, whereas anti-inflammatory cytokines inhibited expression of this lectin or had no considerable effect. Compared with their wild-type counterpart, Gal-1-deficient (Lgals1(-/-)) mice showed enhanced cardiac inflammation, characterized by increased numbers of macrophages, natural killer cells, and total T cells, but reduced frequency of regulatory T cells, leading to impaired cardiac function at baseline and impaired ventricular remodeling 7 days after nonreperfused AMI. Treatment of mice with recombinant Gal-1 attenuated cardiac damage in reperfused AMI. Taken together, our results indicate a protective role for Gal-1 in normal cardiac homeostasis and postinfarction remodeling by preventing cardiac inflammation. Thus, Gal-1 treatment represents a potential novel strategy to attenuate heart failure in AMI.

| S-EPMC5691326 | biostudies-other

Regulatory B cells improve ventricular remodeling after myocardial infarction by modulating monocyte migration.

Project description:Overactivated inflammatory responses contribute to adverse ventricular remodeling after myocardial infarction (MI). Regulatory B cells (Bregs) are a newly discovered subset of B cells with immunomodulatory roles in many immune and inflammation-related diseases. Our study aims to determine whether the expansion of Bregs exerts a beneficial effect on ventricular remodeling and explore the mechanisms involved. Here, we showed that adoptive transfer of Bregs ameliorated ventricular remodeling in a murine MI model, as demonstrated by improved cardiac function, decreased scar size and attenuated interstitial fibrosis without changing the survival rate. Reduced Ly6Chi monocyte infiltration was found in the hearts of the Breg-transferred mice, while the infiltration of Ly6Clo monocytes was not affected. In addition, the replenishment of Bregs had no effect on the myocardial accumulation of T cells or neutrophils. Mechanistically, Bregs reduced the expression of C-C motif chemokine receptor 2 (CCR2) in monocytes, which inhibited proinflammatory monocyte recruitment to the heart from the peripheral blood and mobilization from the bone marrow. Breg-mediated protection against MI was abrogated by treatment with an interleukin 10 (IL-10) antibody. Finally, IL-10 neutralization reversed the effect of Bregs on monocyte migration and CCR2 expression. The present study suggests a therapeutic value of Bregs in limiting ventricular remodeling after MI through decreasing CCR2-mediated monocyte recruitment and mobilization.

| S-EPMC8310480 | biostudies-literature

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