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

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

PROVIDER: PRJNA807633 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18050975.fastq.gz	Fastqsanger.gz
	SRR18050976.fastq.gz	Fastqsanger.gz
	SRR18050977.fastq.gz	Fastqsanger.gz
	SRR18050978.fastq.gz	Fastqsanger.gz
	SRR18050979.fastq.gz	Fastqsanger.gz

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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 (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

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

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

2022-03-31 | GSE196867 | GEO

Macrophage-produced VEGFC is induced by efferocytosis to ameliorate cardiac injury and inflammation.

Project description:Clearance of dying cells by efferocytosis is necessary for cardiac repair after myocardial infarction (MI). Recent reports have suggested a protective role for vascular endothelial growth factor C (VEGFC) during acute cardiac lymphangiogenesis after MI. Here, we report that defective efferocytosis by macrophages after experimental MI led to a reduction in cardiac lymphangiogenesis and Vegfc expression. Cell-intrinsic evidence for efferocytic induction of Vegfc was revealed after adding apoptotic cells to cultured primary macrophages, which subsequently triggered Vegfc transcription and VEGFC secretion. Similarly, cardiac macrophages elevated Vegfc expression levels after MI, and mice deficient for myeloid Vegfc exhibited impaired ventricular contractility, adverse tissue remodeling, and reduced lymphangiogenesis. These results were observed in mouse models of permanent coronary occlusion and clinically relevant ischemia and reperfusion. Interestingly, myeloid Vegfc deficiency also led to increases in acute infarct size, prior to the amplitude of the acute cardiac lymphangiogenesis response. RNA-Seq and cardiac flow cytometry revealed that myeloid Vegfc deficiency was also characterized by a defective inflammatory response, and macrophage-produced VEGFC was directly effective at suppressing proinflammatory macrophage activation. Taken together, our findings indicate that cardiac macrophages promote healing through the promotion of myocardial lymphangiogenesis and the suppression of inflammatory cytokines.

| S-EPMC9057589 | biostudies-literature

High VEGFC expression is associated with unique gene expression profiles and predicts adverse prognosis in pediatric and adult acute myeloid leukemia.

Project description:High VEGFC mRNA expression of AML blasts is related to increased in vitro and in vivo drug resistance. The prognostic significance of VEGFC on long-term outcome and its associated gene expression profiles remain to be defined. We studied the effect of VEGFC on treatment outcome and investigated gene expression profiles associated with VEGFC using microarray data of 525 adult and 100 pediatric AML patients. High VEGFC expression appeared strongly associated with reduced complete remission rate, reduced overall and event-free survival (OS and EFS) in adult AML. Multivariable analysis established high VEGFC as prognostic indicator independent of cytogenetic risk, FLT3-ITD, NPM1, CEBPA, age and WBC. Also in pediatric AML high VEGFC was related to reduced OS. A unique series of differentially expressed genes was identified that distinguished AML with high VEGFC from AML with low VEGFC, i.e., 331 upregulated genes (representative of proliferation, VEGF-receptor activity, signal transduction) and 44 downregulated genes (e.g. related to apoptosis) consistent with a role in enhanced chemoresistance. In conclusion, high VEGFC predicts adverse long-term prognosis and provides prognostic information in addition to well-known prognostic factors. 98 bone marrow and peripheral blood samples were collected at diagnosis and frozen. They were later thawed and hybridized to Affymetrix U133 Plus 2.0 arrays.

2010-06-09 | E-GEOD-22056 | biostudies-arrayexpress

Study of human macrophage reprogramming toward a pro-resolving profile by efferocytosis

Project description:Inﬂammation is a physiopathological process triggered by infection or tissue damage. Immune system initiates coordinated sequential steps in response to these danger signals. Once the threat has been contained inflammation has to be subsequently shut down. Inflammation resolution is initiated by the reprogramming of pro-inflammatory macrophages toward a pro-resolving profile. This reprogramming is induced in particular by the non-phlogistic engulfment of apoptotic cells, mostly apoptotic neutrophils, a process called efferocytosis. As a matter of fact, macrophages are an essential linchpin regulating both inflammation triggering and sustaining and inflammation resolution. This duality can be achieved through the tremendous plasticity of these innate immune cells. Indeed, depending on microenvironmental signals (cytokines, efferocytosis, growth factors…) macrophages can adopt numerous diverse and sometimes antagonistic phenotypes. The mechanisms governing these transitions remain relatively scattered especially in human. With this project we propose to explore the mechanisms involved in human macrophage reprogramming toward a pro-resolving profile after efferocytosis. The stakes are high due to the estimated prevalence of chronic inflammatory diseases in Western society is 5 to 7%. Chronic inflammation is a burden to patient due to life-long debilitating illness and increased mortality and is also a burden to society due to high costs for therapy and care. Finding new therapies to limit chronic inflammation establishment and persistence is thus a highly valuable goal.

2021-12-01 | E-MTAB-8885 | biostudies-arrayexpress

Transcriptional analysis of efferocytosis in mouse skin wounds

Project description:Defects in apoptotic cell clearance, or efferocytosis, can cause inflammatory diseases and prevent tissue repair due in part, to a key role of efferocytosis in inducing a pro-repair transcriptional program in phagocytic cells like macrophages. While the cellular machinery and metabolic pathways involved in efferocytosis have been characterized, the precise efferocytic response of macrophages is dependent on the identity and macromolecular cues of apoptotic cells, and the complex tissue microenvironment in which efferocytosis occurs. Here, we find that macrophages undergoing active efferocytosis in mid-stage mouse skin wounds in vivo display a pro-repair gene program, while efferocytosis of apoptotic skin fibroblasts in vitro induces an immature/inflammatory transcription response. These data provide a resource for understanding how the skin wound niche influences macrophage efferocytosis and will be useful for future investigations that define the role of efferocytosis during tissue repair

2024-08-06 | GSE273754 | GEO

Broad-spectrum antibiotics disrupt homeostatic efferocytosis [scRNA-seq]

Project description:The clearance of apoptotic cells, termed efferocytosis, is essential for tissue homeostasis and prevention of autoimmunity. Although past studies have elucidated local molecular signals that regulate homeostatic efferocytosis1 in a tissue, whether signals arising distally also regulate homeostatic efferocytosis remains elusive. Here, we find that large peritoneal macrophages (LPMs) display impaired efferocytosis in broad-spectrum antibiotics (ABX)-treated, vancomycin-treated, and germ-free mice in vivo. Mechanistically, the microbiota-derived short-chain fatty acid butyrate directly boosted efferocytosis efficiency/capacity in mouse and human macrophages, and rescued ABX-induced LPM efferocytosis defects in vivo. Bulk mRNA sequencing of butyrate-treated macrophages in vitro and single cell mRNA sequencing of LPMs isolated from ABX-treated and butyrate-rescued mice revealed regulation of efferocytosis-supportive transcriptional programs. Specifically, we found that the efferocytosis receptor T-cell immunoglobulin and mucin domain containing 4 (TIM-4, Timd4) was downregulated in LPMs of ABX-treated mice but rescued by oral butyrate and TIM-4 was required for the butyrate-induced enhancement of LPM efferocytosis capacity. LPM efferocytosis was impaired beyond withdrawal of ABX and ABX-treated mice exhibited significantly worse disease in a mouse model of lupus. Our results demonstrate that homeostatic efferocytosis relies on distal metabolic signals and suggest that defective homeostatic efferocytosis may explain link between ABX use and inflammatory disease.

2024-07-16 | GSE270512 | GEO

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