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A subset of temporary resident cardiac macrophages induced by myocardial infarction limits adverse ventricular remodeling [spatial RNA-seq]

ABSTRACT: We provided an analysis of mouse macrophage heterogeneity in the heart after MI using spatial transcriptome sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE219116 | GEO | 2023/10/20

REPOSITORIES: GEO

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A subset of temporary resident cardiac macrophages induced by Myocardial infarction limits adverse ventricular remodeling

Project description:We provided an mRNA-seq analysis of mouse macrophage heterogeneity in the heart after MI.

2023-10-20 | GSE230811 | GEO

A subset of temporary resident cardiac macrophages induced by myocardial infarction limits adverse ventricular remodeling [scRNA-seq]

Project description:We provided a single cell mRNA-seq analyses of mouse macrophage heterogeneity in the heart after MI.

2023-10-20 | GSE216211 | GEO

A subset of temporary resident cardiac macrophages induced by myocardial infarction limits adverse ventricular remodeling

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-10-20 | GSE219117 | GEO

A subset of temporary resident cardiac macrophages induced by myocardial infarction limits adverse ventricular remodeling

Project description:A subset of temporary resident cardiac macrophages induced by myocardial infarction limits adverse ventricular remodeling

| PRJNA907049 | ENA

A subset of temporary resident cardiac macrophages induced by Myocardial infarction limits adverse ventricular remodeling

Project description:A subset of temporary resident cardiac macrophages induced by Myocardial infarction limits adverse ventricular remodeling

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A subset of temporary resident cardiac macrophages induced by myocardial infarction limits adverse ventricular remodeling [spatial RNA-seq]

Project description:A subset of temporary resident cardiac macrophages induced by myocardial infarction limits adverse ventricular remodeling [spatial RNA-seq]

| PRJNA907052 | ENA

A subset of temporary resident cardiac macrophages induced by myocardial infarction limits adverse ventricular remodeling [scRNA-seq]

Project description:A subset of temporary resident cardiac macrophages induced by myocardial infarction limits adverse ventricular remodeling [scRNA-seq]

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Plasma circulating extracellular RNAs in left ventricular remodeling post-myocardial infarction

Project description:Despite substantial declines in mortality following myocardial infarction (MI), subsequent left ventricular remodelling (LVRm) remains a significant long-term complication. Extracellular small non-coding RNAs (exRNAs) have been associated with cardiac inflammation and fibrosis and we hypothesized that they are associated with post-MI LVRm phenotypes. RNA sequencing of exRNAs was performed on plasma samples from patients with “beneficial” (decrease LVESVI ≥20%, n=11) and “adverse” (increase LVESVI ≥15%, n=11) LVRm. Selected differentially expressed exRNAs were validated by RT-qPCR (n=331) and analyzed for their association with LVRm determined by cardiac MRI. Principal components of exRNAs were associated with LVRm phenotypes post-MI; specifically, LV mass, LV ejection fraction, LV end systolic volume index, and fibrosis. We then investigated the temporal regulation and cellular origin of exRNAs in murine and cell models and found that: 1) plasma and tissue miRNA expression was temporally regulated; 2) the majority of the miRNAs were increased acutely in tissue and at sub-acute or chronic time-points in plasma; 3) miRNA expression was cell-specific; and 4) cardiomyocytes release a subset of the identified miRNAs packaged in exosomes into culture media in response to hypoxia/reoxygenation. In conclusion, we find that plasma exRNAs are temporally regulated and are associated with measures of post-MI LVRm.

2019-04-01 | GSE112690 | GEO

Connective Tissue Growth Factor Inhibition Enhances Cardiac Repair and Limits Fibrosis After Myocardial Infarction

Project description:Background. Accumulation of extracellular matrix in the myocardium attenuates cardiac contractile function, and predisposes to arrhythmias and sudden cardiac death. Connective tissue growth factor (CTGF) is a matricellular protein that has been shown to promote development of cardiac fibrosis. Objectives. To investigate for the potential of CTGF monoclonal antibody (CTGF mAb) in protecting from development of cardiac fibrosis following myocardial infarction (MI), and to evaluate its effect during infarct repair and acute cardiac ischemia-reperfusion (I/R) injury. Methods. Mice were subjected to MI or to I/R injury and treated with either control IgG or CTGF mAb. Cultured human cardiac fibroblasts were used to investigate the signalling mechanisms modulated by CTGF mAb. Results. Treatment with CTGF mAb for four days from day three after MI improved survival, attenuated infarct expansion, and resulted in better preserved left ventricular (LV) systolic function. CTGF mAb therapy for six weeks from day seven after MI reduced the MI-induced increase in cardiomyocyte size, heart weight to body weight ratio and remote LV fibrosis. RNA sequencing analysis of LV samples showed that CTGF mAb induced expression of cardiac repair/developmental genes and normalized the MI-induced increase in expression of inflammatory/profibrotic genes. CTGF mAb induced c-Jun N-terminal kinase (JNK) phosphorylation in vivo and in vitro, and inhibition of JNK abrogated the reduced collagen production in CTGF mAb treated fibroblasts. Conclusions. Treatment with CTGF mAb induces expression of cardiac repair/developmental genes and inhibits expression of inflammatory/pro-fibrotic genes in MI hearts providing benefit during post-MI cardiac repair and reducing post-MI cardiac fibrosis.

2019-04-02 | GSE129134 | GEO

Self-renewing resident cardiac macrophages limit adverse remodeling following myocardial infarction

Project description:Mononuclear phagocytes promote injury and repair following myocardial infarction but discriminating functions within mixed populations remains challenging. We utilized fate mapping and single cell RNA-sequencing to delineate fate specification trajectories of heterogeneous cardiac macrophage subpopulations. In steady state, TIMD4 expression tracked with a dominant resident cardiac macrophage subset that persisted via in situ self-renewal with minimal monocyte input. Following ischemic injury, monocytes displayed significant plasticity, ultimately adopting transcriptional states similar to resident macrophages, but also multiple unique states. Ischemic injury reduced resident macrophage abundance within infarct tissue, and despite transcriptional similarity, TIMD4 expression distinguished resident from recruited macrophages. Specific lineage-based depletion of resident cardiac macrophages resulted in depressed cardiac function and adverse remodeling primarily within the peri-infarct zone, the only region of the myocardium where resident macrophages expanded numerically following injury. Together, these data highlight a non-redundant, cardioprotective role of resident cardiac macrophages, and the diverse transcriptional fates recruited monocytes can adopt.

2018-12-15 | GSE119355 | GEO

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