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Rattus norvegicus

ABSTRACT: Genome-wide maps of H3K9me3 and H3K4me3 state in failing heart with or without chaetocin in animal model

PROVIDER: PRJNA284798 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2039160.fastq.gz	Fastqsanger.gz
	SRR2039161.fastq.gz	Fastqsanger.gz
	SRR2039162.fastq.gz	Fastqsanger.gz
	SRR2039163.fastq.gz	Fastqsanger.gz
	SRR2039164.fastq.gz	Fastqsanger.gz

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Genome-wide maps of H3K9me3 and H3K4me3 state in failing heart with or without chaetocin in animal model

Project description:Epigenetic status has been linked to cardiac hypertrophy and heart failure. Histone deacetylase inhibitors are promising drugs for preventing cardiac remodeling. We previously demonstrated very different patterns of histone H3 lysine 9 trimethylation (H3K9me3) and histone H3 lysine 4 trimethylation (H3K4me3) in failing hearts compared to control hearts in both animal models and clinical heart specimens. Here, we focused on a heart failure-specific histone modification, H3K9me3, and investigated the prognostic efficacy of administering a histone H3K9 methyltransferase inhibitor, chaetocin, to Dahl salt-sensitive rats, an animal model of heart failure. Chaetocin delayed the timing of transition from cardiac hypertrophy to heart failure, and prolonged survival in this animal model. Mitochondrial dysfunction was improved with inhibitor use in the failing heart. ChIP-seq analysis demonstrated that heart failure caused an increase in H3K9me3 alignments in thousands of repetitive elements, including regions neighboring mitochondrial genes, and a corresponding reduction of this effect with inhibitor use. However, at 35 loci, heart failure was conversely associated with a reduction in H3K9me3 alignments, and inhibitor use reversed this effect. These data suggest that excessive heterochromatinization of repetitive elements in the failing heart might impair pumping function with mitochondrial gene silencing. H3K9 methyltransferase inhibitors may be a promising novel therapy for chronic heart failure.

2015-05-31 | GSE69194 | GEO

Chaetocin efficacy on Dahl rat

Project description:Transcriptional profiling of left ventricular tissues of Dahl rat with or without treatment of chaetocin Three-condition experiment, Control vs. failing heart, failing heart vs. treatment with chaetocin. 3 samples mixture per each group

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Project description:The conversion of fibroblasts to myotubes by forced expression of MyoD1 is among the earliest demonstrations of reprogramming of vertebrate cell state. To gain insights into the chromatin state of genes required for reprogramming, we profiled H3K4me3, H3K27me3 and H3K9me3. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. ChIP was performed using an antibody against H3K4me3, H3K27me3 and H3K9me3.

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Project description:Chaetocin efficacy on Dahl rat

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Project description:MicroRNA profiling of the failing heart after myocardial infarction induction and doxorubicin treatment

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Project description:We generated genome-wide chromatin-state maps of mouse dendritic cells in steady and dectin-1 activated with or without NFAT inhibitor FK506. We found the differential H3K4me3 signatures in these cells. This study provides the epigenetic signatures of steady, dectin-1activated with or without NFAT inhibition. We also generated stable dendritic cell line D1 expressing a V5 tagging NFAT1. This cell line was used to map the global binding sites of NFAT1 upon dectin-1 activation with 10ug/ml curdlan for 30 minutes. examine NFAT1-v5 genome wide binding sites and differential H3K4me3 epigenetic modification in steady, dectinn-1 activated with or without NFAT inhibiton.

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