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

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

PROVIDER: PRJNA488827 | ENA |

REPOSITORIES: ENA

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	SRR7777113.fastq.gz	Fastqsanger.gz
	SRR7777114.fastq.gz	Fastqsanger.gz

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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

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

Project description:Macrophages promote both injury and repair after myocardial infarction, but discriminating functions within mixed populations remains challenging. Here we used fate mapping, parabiosis and single-cell transcriptomics to demonstrate that at steady state, TIMD4+LYVE1+MHC-IIloCCR2- resident cardiac macrophages self-renew with negligible blood monocyte input. Monocytes partially replaced resident TIMD4-LYVE1-MHC-IIhiCCR2- macrophages and fully replaced TIMD4-LYVE1-MHC-IIhiCCR2+ macrophages, revealing a hierarchy of monocyte contribution to functionally distinct macrophage subsets. Ischemic injury reduced TIMD4+ and TIMD4- resident macrophage abundance, whereas CCR2+ monocyte-derived macrophages adopted multiple cell fates within infarcted tissue, including those nearly indistinguishable from resident macrophages. Recruited macrophages did not express TIMD4, highlighting the ability of TIMD4 to track a subset of resident macrophages in the absence of fate mapping. Despite this similarity, inducible depletion of resident macrophages using a Cx3cr1-based system led to impaired cardiac function and promoted adverse remodeling primarily within the peri-infarct zone, revealing a nonredundant, cardioprotective role of resident cardiac macrophages.

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A Steroid Receptor Coactivator Stimulator (MCB-613) Prevents Adverse Remodeling After Myocardial Infarction

Project description:A Steroid Receptor Coactivator Stimulator (MCB-613) Prevents Adverse Remodeling After Myocardial Infarction

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Myofibroblast-specific 5-HT2B Mediates Adverse Remodeling Following Myocardial Infarction

Project description:Myofibroblast-specific 5-HT2B Mediates Adverse Remodeling Following Myocardial Infarction

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Myofibroblast-specific 5-HT2B Mediates Adverse Remodeling Following Myocardial Infarction

Project description:We report that ablation of the serotonin 2B receptor in periostin-expressing cells improves cardiac structure and function following myocardial infarction. We isolated PDGFRa expressing cells during the fibrotic healing phase after injury, and show that these cells have alterations in the expression of genes controlling cell cycle progression as well as a few markers of cell adhesion and migration.

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Project description:We studied new microRNAs involved in the left ventricular adverse remodeling (LVAR) process after the ST elevation myocardial infarction (STEMI). We analyzed the expression of miRNAs in peripheral blood mononuclear cells (PBMCs) isolated from a group of non-LVAR (n = 5) and LVAR STEMI patients (n = 5), before (0 hour) and after a primary percutaneous coronary intervention (PPCI; 6 hours).

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