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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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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

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

Deletion of cardiac-enriched lncRNA CARDINAL exacerbate TAC induced hypertrophy

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

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

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

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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

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

Differentially Expressed piRNAs in TAC-induced mouse cardiac hypertrophy

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

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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.

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Aberrantly expressed microRNAs participate in cardiac hypertrophy by modulating multiple signaling pathways

Project description:The expressed difference of aberrant microRNAs was successfully constructed through detection in a rat model of cardiac hypertrophy,which had been subjected to transverse aortic constriction surgery. In this study, the expressed situation of aberrant microRNAs was measured in a rat model of cardiac hypertrophy. The survey was contucted in the rats 5, 10, 15 or 20 days later after TAC surgery.

2012-06-08 | E-GEOD-38599 | biostudies-arrayexpress

Expression data of murine model of cardiac hypertrophy

Project description:An initial cellular change in the pathogenesis of heart failure is cardiomyocyte hypertrophy, characterized by increased cell size, enhanced protein synthesis and reactivation of fetal genes. In addition to mechanical stresses, several neurohumoral factors have been identified as potent hypertrophic agents, including angiotensin II, endothelin, and catecholamines. We used microarrays to study the gene expression during cardiac hypertrophy. Balb/c mice (6-8w) were treated with TAC, ATII infusion, and myocardial infarction. TAC model: The transverse aorta (TAC) was constricted at the upper left sternal border by ligation with a 7-silk surgical thread and 27-gauge needle, which was removed thereafter. Sham-operated controls underwent an identical procedure without TAC. At 1 week and 1month after the procedure, LV was harvested. Ang II model.: Ang II was dissolved in 0.9% NaCl at concentrations sufficient to allow an infusion rate of 2.0 mg/kg/day, known to produce hypertension and cardiac hypertrophy. Control mice received a vehicle (saline) via an osmotic minipump. At 1 week after the procedure, LV was harvested. MI model: The proximal portion of the left coronary artery was ligated using an 8-0 nylon thread. Myocardial ischemia was confirmed by the discoloration of the heart and typical ECG changes. After 30 min occlusion, the left coronary artery was reperfused by loosening the ligature. In sham-operated mice (SHAM), the pericardium was opened, but the coronary artery was not ligated. At 1 day, 1week, and 1 month after the procedure, LV was harvested.

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