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Splenic CD169+Tim4+ Marginal Metallophilic Macrophages Are Essential for Wound Healing After Myocardial Infarction

ABSTRACT: Splenic CD169+Tim4+ Marginal Metallophilic Macrophages Are Essential for Wound Healing After Myocardial Infarction

PROVIDER: PRJNA1225298 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR32389108_1.fastq.gz	Fastqsanger.gz
	SRR32389108_2.fastq.gz	Fastqsanger.gz
	SRR32389109_1.fastq.gz	Fastqsanger.gz
	SRR32389109_2.fastq.gz	Fastqsanger.gz

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Splenic CD169+Tim4+ Marginal Metallophilic Macrophages Are Essential for Wound Healing After Myocardial Infarction

Project description:Fidelity of wound healing after myocardial infarction (MI) is an important determinant of subsequent adverse cardiac remodeling and failure. Macrophages derived from infiltrating Ly6Chi blood monocytes are a key component of this healing response; however, the importance of other macrophage populations is unclear. Here, using a variety of in vivo murine models and orthogonal approaches, including surgical myocardial infarction, splenectomy, parabiosis, cell adoptive transfer, lineage tracing and cell tracking, RNA sequencing, and functional characterization, we establish in mice an essential role for splenic CD169+Tim4+ marginal metallophilic macrophages (MMMs) in post-MI wound healing. Splenic CD169+Tim4+ MMMs circulate in blood as Ly6Clow monocytes expressing macrophage markers and help populate CD169+Tim4+CCR2-LYVE1low macrophages in the naïve heart. After acute MI, splenic MMMs augment phagocytosis, CCR3 and CCR4 expression, and robustly mobilize to the heart, resulting in marked expansion of cardiac CD169+Tim4+LyVE1low macrophages with an immunomodulatory and pro-resolving gene signature. These macrophages are obligatory for apoptotic neutrophil clearance, suppression of inflammation, and induction of a reparative macrophage phenotype in the infarcted heart. Splenic MMMs are both necessary and sufficient for post-MI wound healing, and limit late pathological remodeling. Liver X receptor-a agonist-induced expansion of the splenic marginal zone and MMMs during acute MI alleviates inflammation and improves short- and long-term cardiac remodeling. Finally, humans with acute ST-elevation MI also exhibit expansion of circulating CD169+Tim4+ cells, primarily within the intermediate (CD14+CD16+) monocyte population. We conclude that splenic CD169+Tim4+ MMMs are required for pro-resolving and reparative responses after MI and can be manipulated for therapeutic benefit to limit long-term heart failure.

2025-06-18 | GSE289921 | GEO

Splenic CD169+Tim4+ Marginal Zone Metallophilic Macrophages Are Essential for Wound Healing and Resolution of Inflammation After Myocardial Infarction

Project description:Fidelity of wound healing after myocardial infarction (MI) is an important determinant of subsequent adverse cardiac remodeling and failure. Macrophages derived from infiltrating Ly6Chi blood monocytes are a key component of this healing response; however, the importance of other macrophage populations is unclear. Here, we establish in mice an essential role for splenic CD169+Tim4+ marginal metallophilic macrophages (MMMs) in post-MI wound healing. Splenic CD169+Tim4+ MMMs circulate in blood as Ly6Clow cells expressing express core macrophage markers and help populate CD169+Tim4+LYVE1low macrophages in the naïve heart. After acute MI, splenic MMMs augment phagocytosis and robustly mobilize to the heart, resulting in marked expansion of cardiac CD169+Tim4+LyVE1low macrophages with an immunomodulatory and pro-resolving gene signature. These macrophages are obligatory for apoptotic neutrophil clearance, suppression of inflammation, and induction of a reparative macrophage phenotype in the infarcted heart. Splenic MMMs are both necessary and sufficient for post-MI wound healing, and limit late pathological remodeling. Pharmacological expansion of the splenic marginal zone and MMMs during acute MI alleviates inflammation and cardiac remodeling. Finally, humans with acute ST-elevation MI also exhibit expansion of circulating CD169+Tim4+ macrophages. We conclude that splenic CD169+Tim4+ MMMs are required for pro-resolving and reparative responses after MI and can be manipulated for therapeutic benefit to limit long-term heart failure.

2025-06-18 | GSE210798 | GEO

Splenic CD169+Tim4+ Marginal Zone Metallophilic Macrophages Are Essential for Wound Healing and Resolution of Inflammation After Myocardial Infarction

Project description:Splenic CD169+Tim4+ Marginal Zone Metallophilic Macrophages Are Essential for Wound Healing and Resolution of Inflammation After Myocardial Infarction

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Tissue proteomics of splenic marginal zone lymphoma

Project description:Splenic marginal zone lymphoma (SMZL) is a rare chronic B lymphoproliferative disease, whose molecular pathogenesis is still not well established. For the first time a proteomic approach was undertaken to analyse the protein profiles of SMZL tissue. Western blot, immunohistochemical analysis and functional data mining were also performed in order to validate results, classify proteins, and explore their potential relationships. We demonstrated that SMZL is characterized by modulation of proteins related to energetic metabolism and apoptosis pathways. We also reported specific proteins (such as biliverdin reductase A, manganese superoxide dismutase, beta-2 microglobulin, growth factor receptor-bound protein 2, acidic leucine-rich nuclear phosphoprotein 32 family member A, and SET nuclear oncogene) directly involved in NF-kBand BCR pathways, as well as in chromatin remodelling and cytoskeleton. Our findings shed new light on SMZL pathogenesis and provide a basis for the future development of novel biomarkers.

2015-04-23 | PXD001124 | Pride

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Project description:CD169+ macrophages residing in naïve or tumor-draining inguinal lymph nodes revealed their protective role in tumor metastasis

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Project description:Tingible body macrophages (TBMs) exist in lymph node B cell follicles and are responsible for clearing apoptotic B cells. Our data suggests that TBMs are of Cd169-lineage. We isolated cells from Cd169Cre/+.Tdtomatofl/fl reporter mice and transcriptionally profiled them to identify putative TBMs and chacterise their development and function relative to other LN cells of the Cd169 lineage.

2023-02-16 | GSE214060 | GEO

Clostridioides difficile CD169

Project description:Clostridioides difficile CD169 Genome sequencing and assembly

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CD169 is a marker of IFN-γ-stimulated inflammatory macrophages in brain tumor [CT2A]

Project description:Therapies against glioblastoma multiforme (GBM) have been largely ineffective due to the infiltration of immunosuppressive tumor-associated macrophages (TAMs). Recent studies demonstrated that TAMs can also be immune-activating. However, markers differentiating these heterogeneous macrophage populations have not been established. In this study, we identified a subset of macrophages expressing CD169 that promote an anti-tumoral microenvironment in GBM. Using single-cell transcriptome analysis, we found that CD169+ macrophages in human and mouse gliomas produced proinflammatory chemokines, leading to the accumulation of T cells and NK cells. Depletion of CD169+ macrophages shortened the survival of mice with gliomas and reduced the function of antitumor lymphocytes. We show that IFN-γ produced by NK cells was critical for the accumulation of CD169+ macrophages into gliomas. Additionally, CD169 expression on macrophages increased the phagocytosis of apoptotic glioma cells. Our finding suggests that the CD169+ subset of TAMs promotes antitumor immune responses against GBM.

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CD169 is a marker of IFN-γ-stimulated inflammatory macrophages in brain tumor [EGFRviii]

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