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Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway

ABSTRACT: Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway

PROVIDER: PRJNA809698 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18114320.fastq.gz	Fastqsanger.gz
	SRR18114321.fastq.gz	Fastqsanger.gz
	SRR18114322.fastq.gz	Fastqsanger.gz
	SRR18114323.fastq.gz	Fastqsanger.gz
	SRR18114324.fastq.gz	Fastqsanger.gz

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Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway [mRNA-seq]

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Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway [mRNA-seq]

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Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway

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Epicardial transplantation of atrial micrografts

Project description:Ischemic heart disease remains the leading cause of mortality and morbidity worldwide despite improved possibilities in medical care. Alongside interventional therapies, such as coronary artery bypass grafting (CABG), adjuvant tissue-engineered and cell-based treatments can provide regenerative improvement. Unfortunately, most of these advanced approaches require multiple lengthy and costly preparation stages without in turn delivering significant clinical benefit. Here, we investigated the effect of epicardial matrix patch-encased atrial appendage micrografts (AAMs) in a mouse model of myocardial infarction. The matrix-covered AAM patches salvaged the myocardium from infarction-induced functional tissue loss. Fibrosis was attenuated, and site-targeted proteomics revealed AAM patch-activated pathways for angiogenesis and cardiogenesis. The matrix component of the graft further supports functional myocardial recovery by ventricular unloading. The composite epicardial matrix graft encasing AAM micrografts delivers effects desirable for adjuvant cardiac therapy preserving functional cardiac tissue and restricting fibrosis after myocardial infarction.

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Project description:Despite extensive studies on endogenous heart regeneration within the past 20 years, the players involved in initiating early regeneration events are far from clear. Here, we assessed the function of neutrophils, the first-responder cells to tissue damage, during heart regeneration. We detected rapid neutrophil mobilization to the injury site after ventricular amputation, peaking at 1-day post-amputation (dpa) and resolving by 3 dpa. Further analyses indicated neutrophil mobilization coincides with peak epicardial cell proliferation and recruited neutrophils associated with activated, expanding epicardial cells at 1 dpa. Neutrophil depletion inhibited myocardial regeneration and significantly reduced epicardial cell expansion, proliferation, and activation. To explore the molecular mechanism of neutrophils on the epicardial regenerative response, we performed scRNA-seq analysis of 1 dpa neutrophils and identified enrichment of the FGF and ERK signaling pathways. Pharmacological inhibition of FGF signaling indicated its’ requirement for epicardial cell expansion, while neutrophil depletion blocked ERK signaling activation in epicardial cells. Altogether, our studies revealed that neutrophils quickly induce epicardial cells, which later accumulate at the injury site and contribute to heart regeneration.

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