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

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

PROVIDER: PRJNA809701 | ENA |

REPOSITORIES: ENA

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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

Project description:Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway

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

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Project description:We report the application of small-RNA sequencing for high-throughput profiling in mouse epicardial cell (MCEC).

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Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway

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

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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:Epicardial cells are progenitors giving rise to the majority of cardiac fibroblasts, coronary smooth muscle cells, and pericytes during cardiac development, and critically modulating heart morphogenesis and coronary development. An integral phase of epicardial cell fate transition is epithelial-to-mesenchymal transition (EMT), which confers motility and facilitates cell fate transition. We identify a pathway involving protein arginine methyltransferase 1 (PRMT1) and its downstream p53 signaling that drives epicardial EMT and invasion. We show that PRMT1 determines the half-life of p53 through regulating alternative splicing of Mdm4, which is a key controller of p53 degradation. Loss of PRMT1 promotes the expression of Mdm4 short form, which inhibits p53 degradation. Accumulation of p53 subsequently enhances Slug degradation and blocks epicardial EMT. We further demonstrated that the PRMT1-Mdm4-p53 pathway drives epicardial cell fate transition into cardiac fibroblasts, coronary smooth muscle cells and pericytes in vivo, and modulates ventricular morphogenesis and coronary vessel formation. Together, our results establish critical functions of the PRMT1-Mdm4-p53 pathway in epicardial EMT, invasion and cell fate transition.

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