Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Deletion of cardiac-enriched lncRNA CARDINAL exacerbate TAC induced hypertrophy

ABSTRACT: Deletion of cardiac-enriched lncRNA CARDINAL exacerbate TAC induced hypertrophy

PROVIDER: PRJNA868413 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21009236_1.fastq.gz	Fastqsanger.gz
	SRR21009236_2.fastq.gz	Fastqsanger.gz
	SRR21009237_1.fastq.gz	Fastqsanger.gz
	SRR21009237_2.fastq.gz	Fastqsanger.gz
	SRR21009238_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

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.

2024-04-22 | GSE210982 | GEO

Analysis of cardiac-enriched lncRNA CARDINAL in TAC induced hypertrophy

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

| PRJNA868408 | ENA

AAV9-medated cardiac expression of lncRNA CARDINAL ameliorate 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 over-expressed in cardiomyocyte using AAV9 driven by cTNT promoter, ameliorate transaortic constriction (TAC) induced hypertrophy.

2024-04-22 | GSE210983 | GEO

AAV9-medated cardiac expression of lncRNA CARDINAL ameliorate TAC induced hypertrophy

Project description:AAV9-medated cardiac expression of lncRNA CARDINAL ameliorate TAC induced hypertrophy

| PRJNA868412 | ENA

Expression Profiling of Heart (NH, TAC and TAC-R)

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.

2024-07-09 | GSE270186 | GEO

Differentially Expressed piRNAs in TAC-induced mouse cardiac hypertrophy

Project description:To systematically investigate the potential role of piRNA(s) and for the identification of specific piRNA(s) dysregulated in cardiac hypertrophy, we examined the global expression profile of piRNAs in left ventricle samples obtained 4 weeks after TAC surgery in adult mice.

2020-07-24 | GSE153445 | GEO

Differentially Expressed piRNAs in TAC-induced mouse cardiac hypertrophy

Project description:Differentially Expressed piRNAs in TAC-induced mouse cardiac hypertrophy

| PRJNA642739 | ENA

Gene expression profiling of cardiomyocyte-enriched populations isolated from mice subject to transverse aortic constriction (TAC) and treated with BIX-01294 for 1 week

Project description:The role of the histone mehyltrasferase G9a (also known as Ehmt2) in cardiac hypertrophy has not been studied extensively. To address how G9a promotes cardiac hypertrophy, we assessed the gene expression signature defined by G9a in cardiomyocytes (CM) of mice subject to transverse aortic constriction (TAC) for 1 wk, a surgical procedure that causes cardiac hypertrophy following the induction of pressure overload. To this end, we compared the expression profiles of CMs isolated from mice treated with the G9a inhibitor BIX-01294 and control groups (untreated and DMSO-treated mice at baseline and after TAC). The expression profiles were defined by Illumina arrays .

2017-08-30 | GSE93691 | GEO

Transcriptome analysis of mouse cardiac hypertrophy

Project description:RNA-Seq analysis of mouse cardiac transcriptome. Transverse aortic contraction was used to induce cardiac hypertrophy (TAC). To compare wild type and physiological cardiac hypertrophy 'Sendetary' (feeding mouse during 4 weeks) and 'Swim (exercise training to induce the cardiac hypertrophy) samples were analysed.

2012-05-11 | E-MTAB-727 | biostudies-arrayexpress

Analysis of cardiac-enriched lncRNA CARDINAL in TAC induced hypertrophy

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-04-22 | GSE210985 | GEO