GEO DataSets

(Submitter supplied) Treatment of pathological cardiac remodeling and subsequent heart failure represents an unmet clinical need. The well conserved lncRNA H19 shows as powerful therapeutic potential in the treatment of pathological cardiac hypertrophy. H19 is strongly repressed in failing hearts from mice, pigs and humans. Gene therapy using murine but also human H19 strongly attenuated heart failure even when cardiac hypertrophy was already established. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

4 Samples

Download data: BW

(Submitter supplied) Treatment of pathological cardiac remodeling and subsequent heart failure represents an unmet clinical need. The well conserved lncRNA H19 shows as powerful therapeutic potential in the treatment of pathological cardiac hypertrophy. H19 is strongly repressed in failing hearts from mice, pigs and humans. Gene therapy using murine but also human H19 strongly attenuated heart failure even when cardiac hypertrophy was already established. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL13912

6 Samples

Download data: TXT

(Submitter supplied) Left ventricle (LV) cardiac biopsies from patients affected by non-end-stage dilated hypokinetic ischemic cardiomyopathy (HF) where collected during Surgical Ventricular Restoration procedure.

Organism:

Homo sapiens

Type:

Expression profiling by RT-PCR

Platform:

GPL21384

25 Samples

Download data: TXT

(Submitter supplied) Aim - Pathological cardiac remodeling is characterized by cardiomyocyte hypertrophy and fibroblast activation, which can ultimately lead to heart failure (HF). Genome-wide expression analysis on heart tissue has been instrumental for the identification of molecular mechanisms at play. However, these data were based on signals derived from all cardiac cell types. Here we aimed for a more detailed view on molecular changes driving cardiomyocyte hypertrophy and failure to aid in the development of therapies to reverse maladaptive remodeling. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

1 Sample

Download data: TSV, TXT

(Submitter supplied) We compared the transcriptome modified by siRNA-mediated cardiac hypertrophy associated epigenentic regulator (Chaer) with negative control siRNA treated neonatal rat ventricular myocytes with or without phenylephrine treatment. The results suggest that Chaer knockdown broadly blocks the phenylephrine-induced hypertrophic programming of the transcriptome.

Organism:

Rattus norvegicus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18694

4 Samples

Download data: TXT

(Submitter supplied) The role of long noncoding RNA (lncRNA) in adult hearts is unknown; also unclear is how lncRNA modulates nucleosome remodelling. An estimated 70% of mouse genes undergo antisense transcription1, including myosin heavy chain 7 (Myh7), which encodes molecular motor proteins for heart contraction2. Here we identify a cluster of lncRNA transcripts from Myh7 loci and demonstrate a new lncRNA–chromatin mechanism for heart failure. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL15520

2 Samples

Download data: BW, FPKM_TRACKING, TXT

(Submitter supplied) Background: Exercise can induce physiological myocardial hypertrophy (PMH), and former athletes can live 5-6 years longer than nonathletic controls, suggesting a benefit after regression of PMH. We previously reported that regression of pathological myocardial hypertrophy has antihypertrophic effects. Accordingly, we hypothesized that antihypertrophic memory exists even after PMH has regressed, increasing myocardial resistance to subsequent pathological hypertrophic stress. more...

Organism:

Mus musculus

Type:

Non-coding RNA profiling by high throughput sequencing; Expression profiling by high throughput sequencing

Platform:

GPL13112

6 Samples

Download data: CSV

(Submitter supplied) Failure of molecular chaperones to direct the correct folding of newly synthesized proteins leads to the accumulation of misfolded proteins in cells. HSPA4 is a member of the heat shock protein 110 family (HSP110) that acts as a nucleotide exchange factor of HSP70 chaperones. We found that the expression of HSPA4 is upregulated in murine hearts subjected to pressure overload and in failing human hearts. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL13730

6 Samples

Download data: CEL

(Submitter supplied) Identification of genes differentially expressed between the neonatal heart of a genetic rat model of cardiac hypertrophy (the Hypertrophic Heart Rat, HHR) and the control (the Normal Heart Rat, NHR) using Affymetrix GeneChip® Rat Gene 1.0 ST Arrays.

Organism:

Rattus norvegicus

Type:

Expression profiling by array

Platform:

GPL6247

16 Samples

Download data: CEL

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL28457 GPL21103

32 Samples

Download data

(Submitter supplied) 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.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL28457

16 Samples

Download data: CSV

(Submitter supplied) 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.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

16 Samples

Download data: CSV

(Submitter supplied) 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. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

8 Samples

Download data: CSV

(Submitter supplied) This study was to identify lncRNAs responsible for exercise-induced cardiac physiological growth

Organism:

Mus musculus

Type:

Expression profiling by array; Non-coding RNA profiling by array

Platform:

GPL21700

9 Samples

Download data: TXT, XLS

(Submitter supplied) Hypertrophic cardiomyopathy (HCM) is an important cause leading to heart failure. Preserving cardiac function particularly in cardiomyocytes (CMs) is essential for improving prognosis in HCM patients. Therefore, understanding single-cell transcriptome characteristics of CMs in HCM would be indispensable to investigate potential therapeutic targets. We applied single-cell tagged reverse transcription (STRT-seq) approach and obtained 338 CM transcriptomes. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20795

5 Samples

Download data: H5AD

(Submitter supplied) NOT PROVIDED; REQUESTED

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21493

16 Samples

Download data: TXT

(Submitter supplied) Adenosine binds to 4 G protein-coupled receptors located on the cardiomyocyte (A1-R, A2a-R, A2b-R and A3-R) and modulates cardiac function during both ischemia and load-induced stress. While the role of adenosine receptor-subtypes has been well defined in the setting of ischemia-reperfusion, far less is known regarding their roles in protecting the heart during other forms of cardiac stress. We characterized the gene expression profiles of heart from A2a-R over-expressing mice subjected to transverse aortic constriction to study the potential of A2a-R activation to protect from pressure-induced heart failure.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

6 Samples

Download data: CEL

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Other; Expression profiling by high throughput sequencing

Platform:

GPL24247

13 Samples

Download data: BW

(Submitter supplied) To investigate the role of the lncRNA Charme in cardiac differentiation and physiology, total RNA was collected from CharmeWT and CharmeKO hearts RNA-seq analysis was performed on CharmeWT and CharmeKO postnatal hearts

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

5 Samples

Download data: TSV

(Submitter supplied) MATR3 CLIP-seq analysis on embryonal (E15) murine hearts was performed to identify the protein RNA-interactors during murine cardiac development and to characterize the differential binding of the protein in conditon of KO of the lncRNA Charme.

Organism:

Mus musculus

Type:

Other

Platform:

GPL24247

8 Samples

Download data: BED, BW