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

ABSTRACT: The purpose of the study was to compare epicardial transcript abundance between control and Hdac3 knockout (KO) epicardial cells (MEC).

ORGANISM(S): Mus musculus

PROVIDER: GSE197297 | GEO | 2022/02/26

REPOSITORIES: GEO

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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]

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

2022-02-26 | GSE197296 | GEO

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

Project description: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 [miRNA-seq]

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

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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.

2022-02-26 | GSE197298 | GEO

Gene expression profiling of HDAC3-depleted mouse liver rescued with wild-type exogenous HDAC3

Project description:We have shown that intravenous injection of HDAC3 floxed mice with adeno-associated virus (AAV) expressing Cre depletes hepatic HDAC3, upregulates lipogenic gene expression, and causes fatty liver. When AAV-Flag-HDAC3 wild-type (WT) is co-injected along with AAV-Cre, the exogenous HDAC3 is expressed at endogenous levels and can completely rescue fatty liver phenotype. Here we profile transcriptome of the rescued WT livers in comparison with HDAC3-depleted (KO) livers. 4-months old C57BL/6 male mice were co-injected with AAV-Cre or AAV-Cre plus AAV-Flag-HDAC3. Mice were fed ad libitum and harvested at 5 pm (ZT10) at 2-weeks post-injection. Liver total RNA was extracted and hybridized to Affymetrix Mouse Gene 1.0ST array.

2013-11-25 | E-GEOD-49386 | biostudies-arrayexpress

Gene expression profiling of HDAC3-depleted mouse liver rescued with wild-type exogenous HDAC3

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Expression data from mouse heart deficient of HDAC3

Project description:Gene expression changes in the heart of MCH3-KO mouse (HDAC3 f/f, Muscle Creatine Kinase-Cre) versus control WT mouse (HDAC3 f/f). Histone deacetylases (HDACs) play important roles in cardiac development and function. We show here that mice deficient of HDAC3 in heart and skeletabl muscle are relatively normal on normal chow, but develop hypertrophic cardiomyopathy and heart failure that leads to death on high-fat diet. This microarray experiment is to explore the underlying molecular mechanism. Hearts from 6-weeks old WT and MCH3-KO C57BL/6 mice (n=4 in each group, male) on normal chow were subjected to RNA extraction and Affymetrix Mouse Gene 1.0ST analysis.

2011-09-20 | E-GEOD-31251 | biostudies-arrayexpress

PRMT1-Mdm4-p53 pathway controls epicardial invasion and cell fate transition

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.

2020-08-18 | GSE122200 | GEO

Endocardial HDAC3 is required for myocardial trabeculation [miRNA-seq]

Project description:To investigate the microRNA regulated in the endocardial cells, we performed high-throughput profiling analysis using small RNA-Seq data obtained from Hdac3 CRISPR knockout mouse cardiac endothelail cells

2024-03-20 | GSE229659 | GEO

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