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Loss of Lin28a Attenuates Cardiac Hypertrophy Induced by Pressure Overload

ABSTRACT: Loss of Lin28a Attenuates Cardiac Hypertrophy Induced by Pressure Overload

PROVIDER: PRJNA418339 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6291380_1.fastq.gz	Fastqsanger.gz
	SRR6291380_2.fastq.gz	Fastqsanger.gz
	SRR6291381_1.fastq.gz	Fastqsanger.gz
	SRR6291381_2.fastq.gz	Fastqsanger.gz
	SRR6291382_1.fastq.gz	Fastqsanger.gz

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Loss of Lin28a Attenuates Cardiac Hypertrophy Induced by Pressure Overload

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: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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