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Nuclear Deformation Guides Chromatin Reorganization in Cardiac Development and Disease

ABSTRACT: Nuclear Deformation Guides Chromatin Reorganization in Cardiac Development and Disease

PROVIDER: PRJNA739991 | ENA |

REPOSITORIES: ENA

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Nuclear Deformation Guides Chromatin Reorganization in Cardiac Development and Disease

Project description:The purpose of this study was to understand the how the supression of H3K9me3 impacts the phenotype of cardiac cells. Therefore, we compared the mRNA expression profiles of cardiac cells isolated from H3K9M (inducible histone H3.3 lysine-to-methionine mutant) and H3WT (inducibly expressed wild-type H3.3) cells.

2022-07-27 | GSE178674 | GEO

Lineage-specific reorganization of nuclear peripheral heterochromatin and H3K9me2 domains

Project description:Dynamic and regulated organization of chromatin within the 3-dimensional space of the nucleus has been postulated to contribute to gene accessibility, gene expression, and cell fate. Here we define the genome-wide lineage-specific reorganization of nuclear peripheral heterochromatin as a multipotent P19 embryocarcinoma cell adopts either a neural or a cardiac fate. We demonstrate that H3K9me2 marked nuclear peripheral heterochromatin undergoes lineage-specific local reorganization during cell fate determination. Lineage-specific loss of H3K9me2 is associated with spatial repositioning of genomic loci away from the nuclear periphery as shown by high-resolution 3D immuno-fluorescence in situ hybridization (3D immuno-FISH). The lineage-specific repositioning of loci away from the nuclear periphery is not always associated with activation of gene expression, but a subset of these genes is transcriptionally activated. Master regulator Mef2c is specifically repositioned from nuclear periphery during early neurogenic differentiation, but not early cardiogenic differentiation, with associated transcript upregulation. Master regulator Myocd is specifically repositioned during early cardiogenic differentiation, but not early neurogenic differentiation, and is transcriptionally upregulated at later stages of cardiac differentiation. These results provide experimental evidence for lineage-specific regulation of nuclear architecture when the same multipotent progenitor cell adopts distinct fates.

2019-01-24 | GSE121314 | GEO

Dynamic reorganization of nuclear architecture during human cardiogenesis

Project description:Dynamic reorganization of nuclear architecture during human cardiogenesis

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Chromatin architecture reorganization in somatic cell nuclear transfer embryos

Project description:Chromatin architecture reorganization in somatic cell nuclear transfer embryos

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Mouse Cardiac Nuclear Proteome

Project description:Mouse Cardiac Nuclear Proteome

2011-03-18 | PRD000400 | Pride

Dynamic reorganization of nuclear architecture during human cardiogenesis [ATAC-seq]

Project description:Dynamic reorganization of nuclear architecture during human cardiogenesis [ATAC-seq]

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Lineage-specific reorganization of nuclear peripheral heterochromatin and H3K9me2 domains

Project description:Lineage-specific reorganization of nuclear peripheral heterochromatin and H3K9me2 domains

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Dynamic reorganization of nuclear architecture during human cardiogenesis [HiC-seq]

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Dynamic reorganization of nuclear architecture during human cardiogenesis [RNA-seq]

Project description:Dynamic reorganization of nuclear architecture during human cardiogenesis [RNA-seq]

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Cardiac tissue remodeling as a new marker to predict cardiac dysfunction induced by radiotherapy.

Project description:The contribution of radiotherapy, per se, in late cardiotoxicity remains controversial. An experimental model was developed, in which rat hearts were exposed to a range of ionizing radiation doses, to clarify its impact on the development of early cardiac dysfunction. Rat’s hearts were exposed to daily doses of 0.04, 0.3 and 1.2 Gy, for 23 days, achieving cumulative doses of 0.92, 6.9 and 27.6 Gy, respectively. Myocardial deformation, assessed by global longitudinal strain, was impaired (a relative percentage reduction of > 15% from baseline) in a dose-dependent manner. Moreover, by scanning electron microscopy, the microvascular density in the cardiac apex was significantly decreased exclusively at 27.6 Gy dosage. Prior to GLS impairment detection, several tools (qRT-PCR, mass spectrometry and western blot) were used to assess cardiac tissue remodeling. The number/expression of several genes, proteins and KEGG pathways, related to inflammation, fibrosis and cardiac muscle contraction, were found to be differently expressed in the cardiac tissue, according to the cumulative dose. Subclinical cardiac dysfunction occurred in a dose-dependent manner as detected by cardiac tissue remodeling, a predictor of the severity of global longitudinal strain impairment. Moreover, there is no dose threshold below which no myocardial deformation impairment was detected. These findings may contribute to i) develop new markers and explore non-invasive magnetic resonance imaging to assess cardiac tissue remodeling as an early predictor of cardiac dysfunction; ii) improve radiation-based diagnostic and therapeutic cardiac procedures; iii) highlight the need for personalized clinical approaches.

2022-09-08 | PXD033194 | Pride

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