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

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

PROVIDER: PRJNA1125390 | ENA |

REPOSITORIES: ENA

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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.

2024-07-09 | GSE270186 | GEO

Differential expression of circRNAs in the three stages of heart failure in TAC mice

Project description:To identify the role of circRNA on the mouse heart during pressure overload induced heart failure, we have employed circRNA microarray expression profiling as a discovery platform to detect circRNA expression. Samples were collected from the sham group and the pressure overload groups (2, 4 and 8 weeks after TAC), with 2 samples per group. The candidate circRNA that may affect the process of heart failure was screened by comparing the pressure overload groups and the sham group.

2022-03-30 | GSE182912 | GEO

Expression profile of BAT from TAC-operated mice

Project description:To analyze the gene expression profile of BAT in heart failure mice model, we performed whole genome microarray expression profiling using brown adipose tissue (BAT) from mice at 2 weeks after Sham or TAC operation.

2022-08-31 | GSE167095 | GEO

Differential expression of mRNAs in the three stages of heart failure in TAC mice

Project description:To identify the role of mRNA on the mouse heart during pressure overload induced heart failure, we have employed high-throughput sequencing to detect mRNA expression. Samples were collected from the sham group and the pressure overload groups (2, 4 and 8 weeks after TAC), with 2 samples per group. The candidate mRNA that may affect the process of heart failure was screened by comparing the pressure overload groups and the sham group.

2022-03-30 | GSE182985 | GEO

Single-cell mRNA sequencing of TAC-model mouse heart tissue

Project description:We studied the cell compositon of mouse heart by single-cell sequencing on TAC-model mice. Distint subgroups of cardiac muscle, fibroblast cell and endothelial cell were detected. We drawed a cell-cell interaction network using specific expressed ligands and receptors of cells. And we also observed the change of interaction and cell transformation with progress of the disease.

2020-03-10 | GSE120064 | GEO

Expression data from mouse heart post transverse aortic constriction (TAC) -surgery 2 weeks

Project description:Expression data from mouse heart post transverse aortic constriction (TAC) -surgery 2 weeks

| PRJNA525864 | ENA

High-coverage TAC-seq expression

Project description:High-coverage TAC-seq expression

| PRJNA431607 | ENA

Heart mRNA profiles of TAC 8-weeks wild type (WT) and miR-27b-3p knockout mice

Project description:Aim: The heart undergoes pathological remodelling under increased stress and neuronal imbalance. MicroRNAs (miRNAs) are involved in post-transcriptional regulation of genes in cardiac physiology and pathology. However, the mechanisms underlying miRNA-mediated regulation of pathological cardiac remodelling remain to be studied. This study aims to explore the function of endogenous microRNA-27b-3p (miR-27b-3p) in pathological cardiac remodelling. Methods and results: We found that miR-27b-3p expression was elevated in heart of patients with cardiac hypertrophy and in transverse aortic constriction (TAC)-induced cardiac hypertrophy mouse model. MiR-27b-3p-knockout mice showed significantly attenuated cardiac hypertrophy, fibrosis, and inflammation induced by two independent pathological cardiac hypertrophy models, TAC and Angiotensin II (Ang II) perfusion. Transcriptome sequencing analysis revealed that miR-27b-3p deletion significantly downregulated TAC-induced cardiac hypertrophy, fibrosis, and inflammatory genes. We identified fibroblast growth factor 1 (FGF1) as a novel miR-27b-3p target gene in the heart, which was upregulated in miR-27b-3p-null mice. Conclusions: Our study has demonstrated that miR-27b-3p induces pathological cardiac remodelling and suggests that inhibition of endogenous miR-27b-3p or administration of FGF1 might have the potential to suppress cardiac remodelling in a clinical setting.

2022-07-27 | GSE158191 | GEO

Single-cell mRNA sequencing of TAC-model mouse heart tissue

Project description:Single-cell mRNA sequencing of TAC-model mouse heart tissue

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RNA sequence analysis of hearts tissue after C57BL/6 mice subjected to transverse aortic constriction (TAC) and dioscin treatment

Project description:To study the differient expression genes, heart tissues from TAC group and TAC treatment with dioscin group are performed to RNA sequence.

2023-08-01 | GSE181347 | GEO

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