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Analysis of cardiac-enriched lncRNA CARDINAL in TAC induced hypertrophy

ABSTRACT: Analysis of cardiac-enriched lncRNA CARDINAL in TAC induced hypertrophy

PROVIDER: PRJNA868408 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21009205.fastq.gz	Fastqsanger.gz
	SRR21009206.fastq.gz	Fastqsanger.gz
	SRR21009207.fastq.gz	Fastqsanger.gz
	SRR21009208.fastq.gz	Fastqsanger.gz
	SRR21009209.fastq.gz	Fastqsanger.gz

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Deletion of cardiac-enriched lncRNA CARDINAL exacerbate TAC induced hypertrophy

Project description:Pathological cardiac hypertrophy is featured by enhanced protein synthesis. Translation inhibition is effective in treating cardiac hypertrophy, yet with systematic side effect. We identified a cardiac-enriched LncRNA CARDINAL, when deleted, exacerbate transaortic constriction (TAC) induced hypertrophy.

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Differentially Expressed piRNAs in TAC-induced mouse cardiac hypertrophy

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Project description:Transcriptome analysis of RNA samples from whole heart Transverse aortic constriction (TAC) is a well-established method for studying the pathomechanisms of heart failure in animal models of cardiac hypertrophy. A number of studies have shown that the treatment of heart failure in this animal model of cardiac hypertrophy suggests that hypertrophy and fibrosis may be reversible. However, since TAC-release protocols that improve hemodynamics by releasing physical stenosis remain undefined, the histological characteristics and molecular biological regulatory mechanisms of the reversibility of cardiac hypertrophy and fibrosis are unknown. Therefore, this study aimed to establish a TAC release model and investigate the reversibility and plasticity mechanisms of myocardial hypertrophy, fibrosis, and angiogenesis. Four weeks post-TAC surgery, TAC release was conducted by cutting the aortic stenosis sutures. The TAC group exhibited severe myocardial hypertrophy, fibrosis, and increased angiogenesis, along with diastolic dysfunction. Conversely, the TAC-release group showed reduced hypertrophy and fibrosis, and improved diastolic function. Gene expression analysis highlighted Regulator of Calcineurin 1 as a key player in cardiac function and histological changes post-TAC release. Rcan1 knockdown exacerbated myocardial hypertrophy and fibrosis in the TAC-release group. This study sheds light on the functional, structural, and histological changes in the heart induced by TAC release and elucidates some of its regulatory mechanisms.

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