Ontology highlight
ABSTRACT:
PROVIDER: PRJNA857912 | ENA |
REPOSITORIES: ENA
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Project description:Our study introduces a novel animal model featuring a cardiomyocyte-specific, inducible knockout of the Prmt5. The primary aim of this model is to investigate the regulatory mechanisms of PRMT5, the main representative of type II PRMTs. We found that PRMT5 controls Acadvl mRNA splicing and that disruptions in this regulation lead to loss of functional ACADVL and cardiac dysfunction. Importantly, we also show that maintained expression of ACADVL is cardioprotective highlighting a potential therapeutic strategy. The animal model was created using a conditional-ready allele of Prmt5 sourced from the European Mouse Mutant Archive (EMMA, specifically the B6Brd;B6N-Tyrc-Brd Atm1Brd Prmt5tm2a(EUCOMM)WtsiPrmt5 strain). To achieve a conditional knockout, the lacZ reporter was excised using flippase recombinase. The resulting Prmt5loxP/loxP mice were then bred with transgenic mice expressing an inducible Cre recombinase under the control of the alpha-myosin heavy chain promoter (alpha-MHC-MerCreMer), enabling deletion of Prmt5 in cardiomyocytes. We provide RNA-sequencing raw and aligned files for two datasets. The first dataset comprises Ctrl. and cKO left-ventricular cardiac tissue upon treatment with either saline (control) or isoprenaline (ISO). The second dataset comprises isolated cardiomyocyte-specific nuclei of Ctrl. and cKO animals. The model enables a controlled study of PRMT5-intrinsic role in heart pathophysiology, with translational relevance for heart failure. Our methodology, including genetic manipulation and the observation of phenotypic outcomes, paves the way for further exploration into the metabolic underpinnings of cardiac health. The animal model was created using a conditional-ready allele of Prmt5 sourced from the European Mouse Mutant Archive (EMMA, specifically the B6Brd;B6N-Tyrc-Brd Atm1Brd Prmt5tm2a(EUCOMM)WtsiPrmt5 strain). To achieve a conditional knockout, the lacZ reporter was excised using flippase recombinase. The resulting Prmt5loxP/loxP mice were then bred with transgenic mice expressing an inducible Cre recombinase under the control of the alpha-myosin heavy chain promoter (alpha-MHC-MerCreMer), enabling deletion of Prmt5 in cardiomyocytes. We provide RNA-sequencing raw and aligned files for two datasets. The first dataset comprises WT and cKO for treated with either saline (control) or isoprenaline. The second dataset comprises WT and cKO of nuclear fractions of isolated cardiomyocytes. The model enables a controlled study of Prmt5's role in heart physiology and pathology, with the potential to unlock new interventions for heart failure. Our methodology, including genetic manipulation and the observation of phenotypic outcomes, paves the way for further exploration into the metabolic underpinnings of cardiac health.
2026-05-15 | E-MTAB-13594 | biostudies-arrayexpress
Project description:In these experiments, we aimed to investigate the role of cardiomyocyte-specific deletion of the G-quadruplex resolvase Dhx36 in heart development and cardiomyocyte differentiation. To achieve this, we conducted multi-omics analysis using single-nuclei RNA sequencing (RNA-seq) and ATAC sequencing (ATAC-seq) on hearts from postnatal day 7 (PD7) wild-type (WT) and Dhx36 conditional knockout (cKO) mice. Our findings reveal that Dhx36 plays a critical role in the development of the cardiac conduction system (CCS) and in the differentiation of both CCS and working cardiomyocytes
2024-09-15 | E-MTAB-14442 | biostudies-arrayexpress
Project description:In these experiments, we aimed to investigate the role of cardiomyocyte-specific deletion of the G-quadruplex resolvase Dhx36 in heart development and cardiomyocyte differentiation. To achieve this, we conducted multi-omics analysis using single-nuclei RNA sequencing (RNA-seq) and ATAC sequencing (ATAC-seq) on hearts from postnatal day 7 (PD7) wild-type (WT) and Dhx36 conditional knockout (cKO) mice. Our findings reveal that Dhx36 plays a critical role in the development of the cardiac conduction system (CCS) and in the differentiation of both CCS and working cardiomyocytes
2024-09-15 | E-MTAB-14441 | biostudies-arrayexpress
Project description:Cardiac remodeling in response to disease or tissue damage severely impairs heart function. Therefore, the description of the molecular mechanisms responsible is essential for the development of effective therapies. Trbp (Tarbp2) is a multi-functional RNA-binding protein (RBP) that is essential during heart development but its role in the adult heart and cardiac remodeling are unknown. We generated inducible conditional knockout mice to delete Trbp from cardiomyocytes in young adults (Trbp-cKOs). While Trbp-cKO mice did not display a detectable phenotype, under stress conditions induced by transverse aortic constriction (TAC) pressure overload, they rapidly developed severe heart failure; this was associated with maladaptive cardiac remodeling and increased interstitial fibrosis.
2025-01-31 | GSE287292 | GEO
Project description:Genome-wide transcriptomic analyses in left ventricles (LVs) from cardiac-specific miR-150 conditional knockout KO (cKO) mice were performed to identify novel miR-150 targets in the heart.
2021-08-18 | GSE177057 | GEO
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| PRJDB7372 | ENA