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DNA methylation inhibition attenuates pressure overload-induced cardiac hypertrophy in rats

ABSTRACT: DNA methylation inhibition attenuates pressure overload-induced cardiac hypertrophy in rats

PROVIDER: PRJNA437252 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6813880.fastq.gz	Fastqsanger.gz
	SRR6813890.fastq.gz	Fastqsanger.gz
	SRR6813881.fastq.gz	Fastqsanger.gz
	SRR6813891.fastq.gz	Fastqsanger.gz
	SRR6813882.fastq.gz	Fastqsanger.gz

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Pressure-Overload Induced Cardiac Hypertrophy

Project description:Aortic banding is an excellent model system to evaluate the process of development of left ventricular hypertrophy in response to hemodynamic stress. The Affymetrix GeneChip MgU74Av1 was used to analyze expression profiles of mice at different time points after surgical intervention for pressure-overload induced hypertrophy. More information about this model may be obtained at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/band_home.html Keywords = Pressure overload, cardiac hypertrophy Keywords: time-course

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Project description:Pathological cardiac hypertrophy is a major risk factor for the development of heart failure and sudden cardiac death, yet the molecular mechanism of cardiac hypertrophy is not fully understood. Recently, we found that the expression of Lin28a, a RNA-binding protein, was significantly upregulated during the early stages of cardiac hypertrophy. Interestingly, cardiac specific conditional deletion of Lin28a blunted pressure overload-induced cardiac hypertrophic responses. Given that Lin28a can bind to diverse mRNA to regulate their abundance and/or translation, we conducted RNA-seq to profile the cardiac transcriptome alteration without Lin28a under pressure overload. It showed that metabolic pathways, including glycolysis and biosynthetic pathway, were remarkedly affected. Thus, our study identifies Lin28a as a crucial regulator of cardiac hypertrophy via its role in metabolic programming.

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Loss of Lin28a Attenuates Cardiac Hypertrophy Induced by Pressure Overload

Project description:Loss of Lin28a Attenuates Cardiac Hypertrophy Induced by Pressure Overload

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DNA methylation inhibition attenuates pressure overload-induced cardiac hypertrophy in rats

Project description:Inhibitors of DNA methyl transferase (DNMT) might be useful for treating cardiac hypertrophy by preventing de novo methylation and reduced transcription of anti-hypertrophic genes. This approach had been tested, but without a detailed phenotypic and methylation analysis. Here, we subjected rats to pressure overload and treatment with the DNMT inhibitor N-phthalyl-L-tryptophan (RG108) and analysed DNA methylation by cardiomyocyte (CM)-specific reduced representation bisulphite sequencing (RRBS).

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Project description:Pressure overload-induced cardiac hypertrophy was examined in IL-18 knockout and littermate control mice. Keywords: genetic modification / disease model

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Project description:Pressure overload-induced cardiac hypertrophy was examined in IL-18 knockout and littermate control mice. Experiment Overall Design: 4 groups with RNA pooled from 5-6 per group. Role of IL-18 on gene expression in cardiac hypertrophy induced by pressure overload (transaortic constriction)

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Project description:Expression profiling of hearts from FVB males subjected to cardiac pressure overload by transverse aortic constriction (TAC). TAC performed on 8-10 weeks month old males and females. Hearts examined 30 weeks after surgery. Keywords: ordered

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Project description:Pimobendan attenuates pressure overload-induced myocardial hypertrophy by inhibiting the MAPKs pathway

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