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Links from GEO DataSets

Items: 20

1.

Neonatal mice adopt to pressure overload by inducing cardiomyocyte proliferation and angiogenesis

(Submitter supplied) Backgound: Cardiac pressure overload, for example in patients with aortic stenosis, induces irreversible damage in the myocardium leading to cardiac dysfunction, cardiomyocyte hypertrophy and interstitial fibrosis. We therefore hypothesized that insufficient cardiac regeneration might contribute to the progression of pressure overload dependent disease. Here, we aimed to elucidate whether pressure overload in the regenerative stage shortly after birth could lead to a more adaptive cardiac response than in the non-regenerative stage in mice.nTAC in the non-regenerative stage induced cardiac dysfunction, myocardial fibrosis and cardiomyocyte hypertrophy. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
9 Samples
Download data: BW, TXT
Series
Accession:
GSE121308
ID:
200121308
2.

Pressure overload greatly promotes neonatal right ventricular cardiomyocyte proliferation - a new model for heart regeneration study

(Submitter supplied) Background: Current mammalian model for heart regeneration research is limited in apex amputation or myocardium infarction, both of which are controversy. Moreover, RNAseq demonstrated there were a very limited set of differential expressed genes between sham and operation heart in the myocardium infarction model. Here we investigated whether pressure overload in the right ventricle(RV), a common phenomenon in congenital heart disease children, could be a better animal model for heart regeneration study when consider cardiomyocyte(CM) proliferation as the most important index. more...
Organism:
Rattus norvegicus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18694
12 Samples
Download data: TXT
Series
Accession:
GSE139561
ID:
200139561
3.

Gata4 is required for postnatal cardiac function and protection from pressure overload-induced heart failure

(Submitter supplied) An important event in the pathogenesis of heart failure is the development of pathological cardiac hypertrophy. In cultured cardiac cardiomyocytes, the transcription factor Gata4 is required for agonist-induced cardiomyocyte hypertrophy. We hypothesized that in the intact organism Gata4 is an important regulator of postnatal heart function and of the hypertrophic response of the heart to pathological stress. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS2316
Platform:
GPL1261
21 Samples
Download data: CEL
Series
Accession:
GSE5500
ID:
200005500
4.
Full record GDS2316

Gata4 heterozygous mutant heart response to pressure overload

Analysis of pressure-overloaded (PO) heart ventricles of animals heterozygous for the second exon deletion of Gata4, a transcription factor. PO induced by transverse aortic constriction. Results provide insight into the role of Gata4 in the regulation of pathways necessary for cardiac hypertrophy.
Organism:
Mus musculus
Type:
Expression profiling by array, transformed count, 2 strain, 2 stress sets
Platform:
GPL1261
Series:
GSE5500
21 Samples
Download data: CEL
5.

RNA-sequencing of MHC-cycD2 transgenic mice after Transverse Aortic Constriction and Aortocaval Shunt surgery

(Submitter supplied) Expression profiling by high throughput sequencing of mice overexpressing cyclin D2 compared to WT control, and of TG mice after pressure and volume overload
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
18 Samples
Download data: TXT
Series
Accession:
GSE103545
ID:
200103545
6.

Gata4-dependent differentiation of c-Kit+ derived endothelial cells underlies deceptive cardiomyocyte regeneration in the heart

(Submitter supplied) Overall goal: To elucidate the endothelial-specific role of Gata4 signaling in endothelial maturation and vascular maintenance. Purpose of analysis: To generate a transcriptional profile of Gata4-deficient endothelial cells in the adult myocardium under homeostatic conditions.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: XLSX
Series
Accession:
GSE109661
ID:
200109661
7.

Cell-type-specific gene regulatory networks underlying murine neonatal heart regeneration at single-cell resolution

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
12 Samples
Download data: MTX, TSV
Series
Accession:
GSE153481
ID:
200153481
8.

Single cell RNA-seq of neonatal heart regeneration

(Submitter supplied) The adult mammalian heart has limited capacity for regeneration following injury, whereas the neonatal heart can readily regenerate within a short period after birth. Neonatal heart regeneration is orchestrated by multiple cell types intrinsic to the heart, as well as immune cells that infiltrate the heart after injury. To elucidate the transcriptional responses of the different cellular components of the mouse heart following injury, we performed single cell RNA-sequencing on neonatal hearts at various time points following myocardial infarction, and coupled the results with bulk tissue RNA-sequencing data collected at the same time points. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: MTX, TSV
Series
Accession:
GSE153480
ID:
200153480
9.

Single cell ATAC-seq of neonatal heart regeneration

(Submitter supplied) The adult mammalian heart has limited capacity for regeneration following injury, whereas the neonatal heart can readily regenerate within a short period after birth. Neonatal heart regeneration is orchestrated by multiple cell types intrinsic to the heart, as well as immune cells that infiltrate the heart after injury. To elucidate the transcriptional responses of the different cellular components of the mouse heart following injury, we performed single cell RNA-sequencing on neonatal hearts at various time points following myocardial infarction, and coupled the results with bulk tissue RNA-sequencing data collected at the same time points. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
4 Samples
Download data: BED, CSV, H5, MTX, TBI, TSV, TXT
Series
Accession:
GSE153479
ID:
200153479
10.

Mechanistic basis of neonatal heart regeneration revealed by transcriptome and histone modification profiling

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
108 Samples
Download data: BW
Series
Accession:
GSE123868
ID:
200123868
11.

Epigenome profiling of neonatal heart regeneration

(Submitter supplied) Background: The adult mammalian heart has limited capacity for regeneration following injury, whereas the neonatal heart can readily regenerate within a short period after birth. To uncover the molecular mechanisms underlying neonatal heart regeneration, we compared the transcriptomes and epigenomes of regenerative and non-regenerative mouse hearts over a 7-day time period following myocardial infarction. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
72 Samples
Download data: BW
Series
Accession:
GSE123867
ID:
200123867
12.

Transcriptome profiling of neonatal heart regeneration

(Submitter supplied) Background: The adult mammalian heart has limited capacity for regeneration following injury, whereas the neonatal heart can readily regenerate within a short period after birth. To uncover the molecular mechanisms underlying neonatal heart regeneration, we compared the transcriptomes and epigenomes of regenerative and non-regenerative mouse hearts over a 7-day time period following myocardial infarction. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
36 Samples
Download data: TXT
Series
Accession:
GSE123863
ID:
200123863
13.

MBNL1 regulates programmed postnatal switching between regenerative and differentiated cardiac states

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Rattus norvegicus
Type:
Expression profiling by high throughput sequencing; Other
Platforms:
GPL31008 GPL28330 GPL24247
54 Samples
Download data: MTX, TXT
Series
Accession:
GSE246744
ID:
200246744
14.

MBNL1 regulates programmed postnatal switching between regenerative and differentiated cardiac states [ActD RNA-seq]

(Submitter supplied) Background: Discovering determinants of cardiomyocyte maturity will be critical to understanding the maintenance of differentiated states and potentially reawakening endogenous regenerative programs in adult mammalian hearts as a therapeutic strategy. Recent evidence has suggested that forced dedifferentiation paired with oncogene expression is sufficient to drive cardiac regeneration. However, elucidation of endogenous developmental determinants of the switch between regenerative and mature cardiomyocyte cell states is necessary for optimal design of regenerative approaches for heart disease. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL28330
17 Samples
Download data: CSV
Series
Accession:
GSE246743
ID:
200246743
15.

MBNL1 regulates programmed postnatal switching between regenerative and differentiated cardiac states [RIP-seq]

(Submitter supplied) Background: Discovering determinants of cardiomyocyte maturity will be critical to understanding the maintenance of differentiated states and potentially reawakening endogenous regenerative programs in adult mammalian hearts as a therapeutic strategy. Recent evidence has suggested that forced dedifferentiation paired with oncogene expression is sufficient to drive cardiac regeneration. However, elucidation of endogenous developmental determinants of the switch between regenerative and mature cardiomyocyte cell states is necessary for optimal design of regenerative approaches for heart disease. more...
Organism:
Rattus norvegicus
Type:
Other
Platform:
GPL31008
6 Samples
Download data: CSV
Series
Accession:
GSE246742
ID:
200246742
16.

MBNL1 regulates programmed postnatal switching between regenerative and differentiated cardiac states [RNA-seq]

(Submitter supplied) Background: Discovering determinants of cardiomyocyte maturity will be critical to understanding the maintenance of differentiated states and potentially reawakening endogenous regenerative programs in adult mammalian hearts as a therapeutic strategy. Recent evidence has suggested that forced dedifferentiation paired with oncogene expression is sufficient to drive cardiac regeneration. However, elucidation of endogenous developmental determinants of the switch between regenerative and mature cardiomyocyte cell states is necessary for optimal design of regenerative approaches for heart disease. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL28330
27 Samples
Download data: CSV
Series
Accession:
GSE246741
ID:
200246741
17.

MBNL1 regulates programmed postnatal switching between regenerative and differentiated cardiac states [scRNA-seq]

(Submitter supplied) Background: Discovering determinants of cardiomyocyte maturity will be critical to understanding the maintenance of differentiated states and potentially reawakening endogenous regenerative programs in adult mammalian hearts as a therapeutic strategy. Recent evidence has suggested that forced dedifferentiation paired with oncogene expression is sufficient to drive cardiac regeneration. However, elucidation of endogenous developmental determinants of the switch between regenerative and mature cardiomyocyte cell states is necessary for optimal design of regenerative approaches for heart disease. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: MTX, TXT
Series
Accession:
GSE246740
ID:
200246740
18.

Deep RNA sequencing analysis after Malat1 silencing in mouse HL1 cells

(Submitter supplied) We have described role of Malat1 in cardiomyocyte proliferation and binucleation. Data shows regulated genes by LNA mediated silencing of Malat1
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL30172
6 Samples
Download data: TXT
Series
Accession:
GSE200733
ID:
200200733
19.

Comparison of gene expression in cardiac macrophages from P1 or P14 mice 3 days following MI

(Submitter supplied) Myocardial infarction (MI) leads to cardiomyocyte death, which triggers an immune response that clears debris and restores tissue integrity. In the adult heart, the immune system facilitates scar formation, which repairs the damaged myocardium but compromises cardiac function. In neonatal mice, the heart can regenerate fully without scarring following MI; however, this regenerative capacity is lost by P7. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
6 Samples
Download data: TXT
Series
Accession:
GSE54530
ID:
200054530
20.

ATF4 Protects the Heart from Failure by Antagonizing Oxidative Stress

(Submitter supplied) Cellular redox control is maintained by generation of reactive oxygen/nitrogen species balanced by activation of antioxidative pathways. Disruption of redox balance leads to oxidative stress, a central causative event in numerous diseases including heart failure. Redox control in the heart exposed to hemodynamic stress, however, remains to be fully elucidated. Here, we show that production of cardiomyocyte NADPH (nicotinamide adenine dinucleotide phosphate), a key factor in redox regulation, is decreased in pressure overload-induced heart failure. more...
Organism:
Rattus norvegicus; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL14844 GPL13112
24 Samples
Download data: TXT, XLSX
Series
Accession:
GSE187005
ID:
200187005
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