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Links from GEO DataSets

Items: 20

1.

Gene expression profiling of hypertrophic and failing cardiomyocytes identifies new players in heart failure

(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
Series
Accession:
GSE138299
ID:
200138299
2.

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

(Submitter supplied) 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. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL23479
6 Samples
Download data: TXT
Series
Accession:
GSE158191
ID:
200158191
3.

mRNA sequencing of mouse and human heart tissue

(Submitter supplied) We deposit the data of single-cell and bulk-cell rna-seq of normal mouse heart. In addition, we conducted bulk rna-seq in human sample and found that many of the heart remodelling-associated genes we discovered show conserved expression pattern in human hypertrophy and heart failure stage.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL19057 GPL18573
45 Samples
Download data: CSV
Series
Accession:
GSE133054
ID:
200133054
4.

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

(Submitter supplied) 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.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
16 Samples
Download data: CSV, TXT
Series
Accession:
GSE120064
ID:
200120064
5.

Single-cell sequencing reveals the cardio-protective role of overexpressing Cox7B in hypertrophic cardiomyopathy

(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
Series
Accession:
GSE227734
ID:
200227734
6.

Chromatin ImmunoPrecipitation DNA-Sequencing after H19 OE and KD

(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
Series
Accession:
GSE153375
ID:
200153375
7.

Microarray-based transcriptome profiling after H19 KO

(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
Series
Accession:
GSE153344
ID:
200153344
8.

Repurposing an anti-cancer drug for the treatment of hypertrophic heart disease

(Submitter supplied) Coronary microvascular dysfunction combined with maladaptive cardiomyocyte morphology and energetics are major contributors towards heart failure advancement. Thus dually enhancing cardiac angiogenesis and targeting cardiomyocyte function to slow, or reverse, the development of heart failure is a logical step towards improved therapy. We present evidence for the potential to repurpose a former anti-cancer Arg-Gly-Asp (RGD)-mimetic pentapeptide, Cilengitide, here used at low doses. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
15 Samples
Download data: TXT
Series
Accession:
GSE127854
ID:
200127854
9.

Combined miRNA and mRNA Sequencing Identifies Protective Transcriptional Signature of Enhanced PI3Kalpha Signaling in Cardiac Hypertrophy

(Submitter supplied) A molecular and bioinformatic pipeline permitting comprehensive analysis and quantification of myocardial miRNA and mRNA expression with next-generation sequencing was developed and the impact of enhanced PI3Kalpha signaling on the myocardial transcriptome signature of pressure overload-induced pathological hypertrophy was explored.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
Platform:
GPL13112
27 Samples
Download data: TXT
Series
Accession:
GSE35350
ID:
200035350
10.

Disruption of Actin Dynamics Regulated by Rho Effector mDia1 Attenuates Pressure Overload-Induced Cardiac Hypertrophic Responses and Exacerbates Dysfunction

(Submitter supplied) Aims: Cardiac hypertrophy is a compensatory response to pressure overload, leading to heart failure. Recent studies have demonstrated that Rho is immediately activated in left ventricles after pressure overload, and that Rho signaling plays crucial regulatory roles in actin cytoskeleton rearrangement during cardiac hypertrophic responses. However, the mechanisms by which Rho and its downstream proteins control actin dynamics during hypertrophic responses remain not fully understood. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL10787
2 Samples
Download data: TXT
Series
Accession:
GSE142697
ID:
200142697
11.

miRNA expression data from CITED4 knockout and control mouse hearts after transverse aortic constriction

(Submitter supplied) To investigate the role of CITED4 in a murine model of cardiac pressure overload
Organism:
Mus musculus
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL17021
10 Samples
Download data: TXT
Series
Accession:
GSE150293
ID:
200150293
12.

Loss of heat shock protein HSPA4 aggravates pressure overload-induced myocardial damage

(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
Series
Accession:
GSE32885
ID:
200032885
13.

Genetic dissection of a super enhancer controlling the Nppa-Nppb cluster in the heart

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Other
Platform:
GPL16417
21 Samples
Download data: WIG
Series
Accession:
GSE158735
ID:
200158735
14.

Genetic dissection of a super enhancer controlling the Nppa-Nppb cluster in the heart after cardiac stress

(Submitter supplied) High-resolution chromosome conformation capture-sequencing of wildtype mice left ventricle after cardiac stress (i.e. hypertrophy and myocardial infarction)
Organism:
Mus musculus
Type:
Other
Platform:
GPL16417
9 Samples
Download data: WIG
Series
Accession:
GSE158708
ID:
200158708
15.

Genetic dissection of a super enhancer controlling the Nppa-Nppb cluster in the heart of RE3 mutants

(Submitter supplied) High-resolution chromosome conformation capture-sequencing of RE3 homozygous mutants
Organism:
Mus musculus
Type:
Other
Platform:
GPL16417
12 Samples
Download data: WIG
Series
Accession:
GSE155140
ID:
200155140
16.

Genetic dissection of a super enhancer controlling the Nppa-Nppb locus in the heart (CUT&RUN)

(Submitter supplied) CUT&RUN H3K27ac PCM-1 sorted left ventricle of Nppa-Nppb double-knockout
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: BED, BIGWIG
Series
Accession:
GSE146734
ID:
200146734
17.

Genetic dissection of a super enhancer controlling the Nppa-Nppb locus in the heart (RNA-Seq)

(Submitter supplied) Whole transcriptome expression analysis of RE1-deficient mice
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
8 Samples
Download data: XLSX
Series
Accession:
GSE146732
ID:
200146732
18.

BET bromodomain inhibition

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL17021 GPL16791
33 Samples
Download data
Series
Accession:
GSE96566
ID:
200096566
19.

Gene expression profile during cardiac stress induced by transverse aortic constriction (TAC) and myocardial infarction (MI) with or without BET protein inhibitor JQ1 in mouse hearts

(Submitter supplied) Purpose: to reveal cardiac stress-inducible genes that are attnuated by BET inhibition
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
21 Samples
Download data: TXT
Series
Accession:
GSE96561
ID:
200096561
20.

Effect of BET bromodomain inhibition with JQ1 in stressed human derived iPS cardiomyocytes

(Submitter supplied) Gene expression profile of endothelin-1 (ET-1) stressed human derived iPS cardiomyocytes (from Cellular Dynamics) with or without the BET bromodomain inhibitor JQ1
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: TXT
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