GEO DataSets

(Submitter supplied) Heart failure is driven by the interplay between master regulatory transcription factors and dynamic alterations in chromatin structure. Coordinate activation of developmental, inflammatory, fibrotic and growth regulators underlies the hallmark phenotypes of pathologic cardiac hypertrophy and contractile failure. While transactivation in this context is known to be associated with recruitment of histone acetyl-transferase enzymes and local chromatin hyperacetylation, the role of epigenetic reader proteins in cardiac biology is unknown. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL13112 GPL9250

13 Samples

Download data: WIG

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

Organism:

Mus musculus; Rattus norvegicus

Type:

Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing

4 related Platforms

60 Samples

Download data: CEL, WIG

(Submitter supplied) Heart failure (HF) is driven via interplay between master regulatory transcription factors and dynamic alterations in chromatin structure. While pathologic gene transactivation in this context is known to be associated with recruitment of histone acetyl-transferases and local chromatin hyperacetylation, the role of epigenetic reader proteins in cardiac biology is unknown. We therefore undertook a first study of acetyl-lysine reader proteins, or bromodomains, in HF. more...

Organism:

Rattus norvegicus

Type:

Expression profiling by array

Platform:

GPL1355

20 Samples

Download data: CEL

(Submitter supplied) Heart failure (HF) is driven via interplay between master regulatory transcription factors and dynamic alterations in chromatin structure. While pathologic gene transactivation in this context is known to be associated with recruitment of histone acetyl-transferases and local chromatin hyperacetylation, the role of epigenetic reader proteins in cardiac biology is unknown. We therefore undertook a first study of acetyl-lysine reader proteins, or bromodomains, in HF. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

27 Samples

Download data: CEL

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

Organism:

Homo sapiens; Mus musculus

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL16791 GPL17021

33 Samples

Download data

(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

(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

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

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing

Platforms:

GPL19057 GPL21493 GPL24247

47 Samples

Download data: BW, CGMAP, TAR

(Submitter supplied) Heart failure can be induced or ameliorated by regulation of chromatin modifying enzymes. Because so many chromatin factors regulate gene expression, we used ATAC-seq to report the status of a given locus at any time—the sum total of all epigenetic modifiers—in a mouse model of pressure overload hypertrophy. Early compensation of pressure overload at 3 days was associated with widespread changes in chromatin accessibility and DNA methylation, the majority of which persisted to the decompensated phase (3 weeks), revealing the temporal nature of epigenomic compensation to pathologic stimuli. more...

Organism:

Mus musculus

Type:

Methylation profiling by high throughput sequencing

Platforms:

GPL24247 GPL21493

23 Samples

Download data: CGMAP

(Submitter supplied) Heart failure can be induced or ameliorated by regulation of chromatin modifying enzymes. Because so many chromatin factors regulate gene expression, we used ATAC-seq to report the status of a given locus at any time—the sum total of all epigenetic modifiers—in a mouse model of pressure overload hypertrophy. Early compensation of pressure overload at 3 days was associated with widespread changes in chromatin accessibility and DNA methylation, the majority of which persisted to the decompensated phase (3 weeks), revealing the temporal nature of epigenomic compensation to pathologic stimuli. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

12 Samples

Download data: TAR

(Submitter supplied) Heart failure can be induced or ameliorated by regulation of chromatin modifying enzymes. Because so many chromatin factors regulate gene expression, we used ATAC-seq to report the status of a given locus at any time—the sum total of all epigenetic modifiers—in a mouse model of pressure overload hypertrophy. Early compensation of pressure overload at 3 days was associated with widespread changes in chromatin accessibility and DNA methylation, the majority of which persisted to the decompensated phase (3 weeks), revealing the temporal nature of epigenomic compensation to pathologic stimuli. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

12 Samples

Download data: BW

(Submitter supplied) Small molecule inhibitors of the acetyl-histone binding protein BRD4 have been shown to block cardiac fibrosis in pre-clinical models of heart failure (HF). However, the mechanisms by which BRD4 promotes pathological myocardial fibrosis remain unclear. Here, we demonstrate that BRD4 functions as an effector of TGF-b signaling to stimulate conversion of quiescent cardiac fibroblasts into Periostin (Postn)-positive cells that express high levels of extracellular matrix. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

10 Samples

Download data: TXT, XLS

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

Organism:

Mus musculus; Rattus norvegicus

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL14844 GPL21103 GPL18694

25 Samples

Download data: BED, WIG

(Submitter supplied) Small molecule inhibitors of the acetyl-histone binding protein BRD4 have been shown to block cardiac fibrosis in pre-clinical models of heart failure (HF). However, the mechanisms by which BRD4 promotes pathological myocardial fibrosis remain unclear. Here, we demonstrate that BRD4 functions as an effector of TGF-b signaling to stimulate conversion of quiescent cardiac fibroblasts into Periostin (Postn)-positive cells that express high levels of extracellular matrix. more...

Organism:

Rattus norvegicus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18694

9 Samples

Download data: TXT

(Submitter supplied) Small molecule inhibitors of the acetyl-histone binding protein BRD4 have been shown to block cardiac fibrosis in pre-clinical models of heart failure (HF). However, the mechanisms by which BRD4 promotes pathological myocardial fibrosis remain unclear. Here, we demonstrate that BRD4 functions as an effector of TGF-b signaling to stimulate conversion of quiescent cardiac fibroblasts into Periostin (Postn)-positive cells that express high levels of extracellular matrix. more...

Organism:

Rattus norvegicus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL14844

6 Samples

Download data: BED, WIG

(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; Other

Platforms:

GPL13112 GPL21103

17 Samples

Download data: GTF, HIC, NARROWPEAK

(Submitter supplied) Understanding the principles of endogenous chromatin structure has key implications for epigenetic therapy. To determine the mechanisms of genome structure-function in post-mitotic cells, genome-wide chromatin conformation capture was performed in cardiac myocytes, a non-dividing, differentiated cell responsible for cardiac contraction. Cardiac-specific CTCF knockout mice demonstrated that loss of CTCF had minimal effect on topologically associating domains; however, it selectively altered boundary strength and A/B compartmentalization, with gene expression changes mimicking those in heart failure. more...

Organism:

Mus musculus

Type:

Other

Platform:

GPL21103

3 Samples

Download data: HIC

(Submitter supplied) Understanding the principles of endogenous chromatin structure has key implications for epigenetic therapy. To determine the mechanisms of genome structure-function in post-mitotic cells, genome-wide chromatin conformation capture was performed in cardiac myocytes, a non-dividing, differentiated cell responsible for cardiac contraction. Cardiac-specific CTCF knockout mice demonstrated that loss of CTCF had minimal effect on topologically associating domains; however, it selectively altered boundary strength and A/B compartmentalization, with gene expression changes mimicking those in heart failure. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL13112

4 Samples

Download data: NARROWPEAK

(Submitter supplied) Understanding the principles of endogenous chromatin structure has key implications for epigenetic therapy. To determine the mechanisms of genome structure-function in post-mitotic cells, genome-wide chromatin conformation capture was performed in cardiac myocytes, a non-dividing, differentiated cell responsible for cardiac contraction. Cardiac-specific CTCF knockout mice demonstrated that loss of CTCF had minimal effect on topologically associating domains; however, it selectively altered boundary strength and A/B compartmentalization, with gene expression changes mimicking those in heart failure. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

10 Samples

Download data: GTF

(Submitter supplied) Hypertrophic cardiomyopathy (HCM) is one of the most frequent inherited heart condition and a well-established risk factor for cardiovascular mortality worldwide. Although hypertrophy is traditionally regarded as an adaptive response to increased workload caused by physiological or pathological stress, prolonged hypertrophy can lead to heart failure characterized by impaired systolic function, increased apoptosis, fibrosis, ventricular dilation, and impaired metabolic substrate flexibility. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

10 Samples

Download data: TXT