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The role of microRNA-204 in pressure overload-induced cardiac hypertrophy

ABSTRACT: The role of microRNA-204 in pressure overload-induced cardiac hypertrophy

PROVIDER: PRJNA769737 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16264602_1.fastq.gz	Fastqsanger.gz
	SRR16264602_2.fastq.gz	Fastqsanger.gz
	SRR16264603_1.fastq.gz	Fastqsanger.gz
	SRR16264603_2.fastq.gz	Fastqsanger.gz
	SRR16264604_1.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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The role of microRNA-204 in pressure overload-induced cardiac hypertrophy

Project description:microRNAs regulate cardiac hypertrophy development, which predicts the risk of heart failure. Here we investigate the role of microRNA-204-5p (miR-204) in developing cardiac hypertrophy and cardiac dysfunction following transaortic constriction. To determine the role of miR-204, we determined the transcriptomic profile of hearts following transaortic constriction.

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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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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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Gene and exon expression change in cardiac hypertrophy with pressure overload

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Gene and exon expression change in cardiac hypertrophy with pressure overload

Project description:Pathological cardiac hypertrophy was induced by pressure overload on the heart. We performed genome-wide exon array experiments with left ventricles of mice with 1 week and 4 week of transverse aortic constriction (TAC). The exon level analysis revealed widespread regulation of alternative splicing and alternative polyadenylation during hypertrophy. Exon and gene expression changes were examined in 1 week and 4 week TAC-operated hearts compared to sham-operated hearts. We used C57/BL6 wildtype mice, and their left ventricles were subject to surgery (each n=2).

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