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Mus musculus

ABSTRACT: Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure [ChIP-seq]

PROVIDER: PRJNA379888 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5349560.fastq.gz	Fastqsanger.gz
	SRR5349561.fastq.gz	Fastqsanger.gz
	SRR5349562.fastq.gz	Fastqsanger.gz
	SRR5349559.fastq.gz	Fastqsanger.gz

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Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure

Project description:Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure

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Project description:Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure [RNA-seq]

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Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure [HiC-seq]

Project description:Understanding the principles of endogenous chromatin structure has key implications for epigenetic therapy. To determine the mechanisms of genome structure-function in post-mitotic cells, genome-wide chromatin conformation capture was performed in cardiac myocytes, a non-dividing, differentiated cell responsible for cardiac contraction. Cardiac-specific CTCF knockout mice demonstrated that loss of CTCF had minimal effect on topologically associating domains; however, it selectively altered boundary strength and A/B compartmentalization, with gene expression changes mimicking those in heart failure. Loss of CTCF (or subjecting wild-type mice to clinically relevant pressure overload stress) remodeled long-range chromatin looping to alter 3D proximity of enhancers and disease causing genes. Depletion of CTCF was sufficient to induce heart failure in mice and human heart failure patients receiving mechanical unloading to attenuate disease progression show increased CTCF expression. These findings establish CTCF in the maintenance of chromatin looping and identify global chromatin remodeling as a causative factor in heart failure.

2017-08-30 | GSE96692 | GEO

Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure [ChIP-seq]

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Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure [RNA-seq]

2017-08-30 | GSE96690 | GEO

Effects of Post-Myocardial Infarction Heart Failure on the Bone Vascular Niche (Mouse Data)

Project description:We demonstrate an age-independent loss of type H bone endothelium in heart failure after myocardial infarction in both mice and in humans. Using single-cell RNA sequencing, we delineate the transcriptional heterogeneity of human bone marrow endothelium showing increased expression of inflammatory genes, including IL1B and MYC, in ischemic heart failure. Endothelial-specific overexpression of MYC was sufficient to induce type H bone endothelial cells, whereas inhibition of NLRP3-dependent IL-1 production partially prevents the post-myocardial infarction loss of type H vasculature in mice.

2021-05-13 | E-MTAB-10448 | biostudies-arrayexpress

Effects of Post-Myocardial Infarction Heart Failure on the Bone Vascular Niche (Human Data)

2021-05-11 | E-MTAB-10432 | biostudies-arrayexpress

Mitotic bookmarking by CTCF and fast post-mitotic gene reactivation in ES cells

Project description:Mitotic bookmarking by CTCF and fast post-mitotic gene reactivation in ES cells

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Gene profiling of Hand2 target genes and transcriptional regulation of Hand2 expression in the postnatal myocardium

Project description:In humans, cardiac hypertrophy is the principal risk factor for the development of overt heart failure and sudden cardiac death from lethal arrhythmias. Although aberrant reactivation of fetal² gene programs is intricately linked to maladaptive hypertrophy of postnatal cardiomyocytes, loss of cardiac function and heart failure, the transcription factors driving these gene programs remain ill defined. We report that the basic helix-loop-helix (bHLH) transcription factor dHAND/Hand2 is re-expressed in the mammalian postnatal myocardium in response to stress signaling. Interestingly, mutant mice overexpressing Hand2 in otherwise healthy ventricular myocytes developed a phenotype of pathological hypertrophy. In contrast, conditional gene-targeted Hand2 mice demonstrated a marked resistance to pressure overload-induced hypertrophy, fibrosis, ventricular dysfunction and induction of a fetal gene program. These data suggest a critical role for the Hand2 transcription factor during hypertrophic remodeling and heart failure. To gain more mechanistically insight in the processes underlying heart failure, we here identified Hand2 target genes by microarray gene expression profiling. RNA samples were collected 4 weeks after sham or TAC surgery (to induce pressure overload) of both tamoxifen-treated Hand2f/f (WT) and MCM-Hand2f/f (KO) mice.

2013-11-15 | E-MTAB-1821 | biostudies-arrayexpress

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