GEO DataSets

Analysis of hearts after acute or chronic induction of a transgenic Akt1 kinase. Acute activation results in reversible hypertrophy, while chronic activation induces transition to failure. Results provide insight into the mechanisms involved in the development of cardiac hypertrophy and failure.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 5 protocol sets

Platform:

GPL339

Series:

GSE3383

18 Samples

Download data

(Submitter supplied) To investigate molecular mechanisms involved in the development of cardiac hypertrophy and heart failure, a tetracycline-regulated transgenic system to conditionally switch a constitutively-active form of the Akt1 protein kinase on or off in the adult heart was developed. Short-term activation (2 weeks) of Akt1 resulted in completely reversible hypertrophy with maintained contractility. In contrast, chronic Akt1 activation (6 weeks) induced extensive cardiac hypertrophy, severe contractile dysfunction, and massive interstitial fibrosis. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Datasets:

GDS2304 GDS2308

Platforms:

GPL339 GPL340

36 Samples

Download data

Analysis of hearts after acute or chronic induction of a transgenic Akt1 kinase. Acute activation results in reversible hypertrophy, while chronic activation induces transition to failure. Results provide insight into the mechanisms involved in the development of cardiac hypertrophy and failure.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 5 protocol sets

Platform:

GPL340

Series:

GSE3383

18 Samples

Download data

(Submitter supplied) Myoglobin knockout mice (myo-/-) adapt to the loss of myoglobin by the activation of a variety of compensatory mechanisms on the structural and functional level. In order to analyze to what extent myo-/- mice would tolerate cardiac stress we used the model of chronic isoproterenol application to induce cardiac hypertrophy in myo-/- mice and wild type (WT) controls. After 14 d of isoproterenol infusion cardiac hypertrophy in WT and myo-/- mice reached a similar level. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL8600

16 Samples

Download data: GPR

(Submitter supplied) Myoglobin knockout mice (myo-/-) adapt to the loss of myoglobin by the activation of a variety of compensatory mechanisms on the structural and functional level. In order to analyze to what extent myo-/- mice would tolerate cardiac stress we used the model of chronic isoproterenol application to induce cardiac hypertrophy in myo-/- mice and wild type (WT) controls. After 14 d of isoproterenol infusion cardiac hypertrophy in WT and myo-/- mice reached a similar level. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL8599

16 Samples

Download data: GPR

(Submitter supplied) We performed microarray analyses on RNA from mice with isoproterenol-induced cardiac hypertrophy and mice with exercise-induced physiological hypertrophy and identified 865 and 2,534 genes that were significantly altered in pathological and physiological cardiac hypertrophy models, respectively.

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS3596

Platform:

GPL1261

9 Samples

Download data: CEL

Comparison of hearts of C57BL/6 males with isoproterenol-induced cardiomyopathy to those with exercise-induced cardiac hypertrophy. Results provide insight into the molecular differences between pathological and physiological cardiac hypertrophy models.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 3 protocol sets

Platform:

GPL1261

Series:

GSE18801

9 Samples

Download data: CEL

(Submitter supplied) We recently introduced a modification of the established monocrotaline (MCT) model for pulmonary hypertension (PH) and subsequent right ventricular (RV) hypertrophy, which allows for the selective induction of either a compensate or decompensated RV hypertrophic phenotype within four weeks after a single subcutaneous MCT injection. Both doses of 30 or 80 mg/kg body weight lead to an intermediate phase of compensated RV hypertrophy (day 14-19), while the former dose leads to a stable compensated phenotype (HYP) and the latter dose progresses towards decompensated ventricular hypertrophy and RV failure (CHF) around day 25-28 (Buermans et. more...

Organism:

Rattus norvegicus

Type:

Expression profiling by array

Dataset:

GDS1928

Platform:

GPL1397

27 Samples

Download data: IMAGENE

(Submitter supplied) 14 days after a single subcutaneous monocrotaline (MCT) injection we isolated the left and right ventricles from wistar rats. Factor1: Comparison between control (CON), compensated hypertrophy (HYP), and decompensated hypertrophy (CHF). Factor2: Comparison between left ventricle (LV) and right ventricle (RV). Keywords: dose response

Organism:

Rattus norvegicus

Type:

Expression profiling by array

Dataset:

GDS742

Platform:

GPL1397

24 Samples

Download data

Temporal analysis of right ventricles at the onset of compensated or decompensated right ventricular hypertrophy. Compensated and decompensated phenotypes induced by injection with 30 and 80 mg/kg monocrotaline, respectively. Results identify potential prognostic markers and therapeutic targets.

Organism:

Rattus norvegicus

Type:

Expression profiling by array, log2 ratio, 3 disease state, 3 time sets

Platform:

GPL1397

Series:

GSE3675

27 Samples

Download data: IMAGENE

Analysis of compensated and decompensated hypertrophies induced by monocrotaline in Wistar. Left and right heart ventricles examined 14 days after monocrotaline injection. Decompensated hypertrophy is a prelude to chronic heart failure.

Organism:

Rattus norvegicus

Type:

Expression profiling by array, log ratio, 3 disease state, 2 tissue sets

Platform:

GPL1397

Series:

GSE1652

24 Samples

Download data

(Submitter supplied) Microarray analysis of gene expression after transverse aortic constriction in mice: comparison of TAC vs. sham group at 48 hours, 10 days, and 3 weeks. Keywords: time-course

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS794

Platform:

GPL81

26 Samples

Download data: CEL, EXP

Expression profiling of hearts from FVB males subjected to cardiac pressure overload by transverse aortic constriction (TAC). TAC performed on 3 month old males. Hearts examined 2, 10, and 21 days after surgery. Results provide insight into the progression of cardiac hypertrophy.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 protocol, 3 time sets

Platform:

GPL81

Series:

GSE1621

26 Samples

Download data: CEL, EXP

(Submitter supplied) We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy. To determine the role of CHF1/Hey2 in pressure overload hypertrophy, we performed ascending aortic banding on wild type and transgenic mice overexpressing CHF1/Hey2 in the myocardium. We found that both wild type and transgenic mice developed increased ventricular weight to body weight ratios one week after aortic banding. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

8 Samples

Download data: CEL

(Submitter supplied) Energy Substrate Uptake and Metabolism are Preserved in Hypertrophic Caveolin-3 Knockout Hearts Keywords: gene knockout

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS3552

Platform:

GPL1261

6 Samples

Download data: CEL

Analysis of hearts lacking caveolin-3 (Cav3), the primary protein component of caveolae in muscle cells. Cav3 deficiency leads to cardiac hypertrophy and contractile dysfunction. Results provide insight into the molecular mechanisms underlying cardiac hypertrophy induced by Cav3 deficiency.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 genotype/variation sets

Platform:

GPL1261

Series:

GSE10848

6 Samples

Download data: CEL

(Submitter supplied) Cardiac-specific PPARalpha transgenic (Tg-PPARalpha) mice show mild cardiac hypertrophy and systolic dysfunction. The failing heart phenotypes observed in Tg-PPARalpha are exacerbated by crossing with cardiac-specific Sirt1 transgenic (Tg-Sirt1) mice, whereas Tg-Sirt1 mice themselves do not show any cardiac hypertrophy or systolic dysfunction. To investigate the mechanism leading to the failing heart phenotypes in TgPPARalpha/Tg-Sirt1 bigenic mice, microarray analyses were performed. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

8 Samples

Download data: CEL

(Submitter supplied) Cardiac hypertrophy has been well-characterized at the level of transcription. During cardiac hypertrophy, genes normally expressed primarily during fetal heart development are re-expressed, and this fetal gene program is believed to be a critical component of the hypertrophic process. Recently, alternative splicing of mRNA transcripts has been shown to be temporally regulated during heart development, leading us to consider whether fetal patterns of splicing also reappear during hypertrophy.We hypothesized that patterns of alternative splicing occurring during heart development are recapitulated during cardiac hypertrophy. more...

Organism:

Rattus norvegicus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL10669

9 Samples

Download data: TXT

(Submitter supplied) Muscle ring finger-1 (MuRF1) is a muscle-specific protein implicated in the regulation of cardiac myocyte size and contractility. MuRF2, a closely related family member, redundantly interacts with protein substrates, and hetero-dimerizes with MuRF1. Mice lacking either MuRF1 or MuRF2 are phenotypically normal whereas mice lacking both proteins develop a spontaneous cardiac and skeletal muscle hypertrophy indicating cooperative control of muscle mass by MuRF1 and MuRF2. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL2876

19 Samples

Download data: GPR

(Submitter supplied) Background: Skeletal muscle constitutes a significant portion of total body mass and is a major regulator of systemic metabolism as it serves as the major site for glucose disposal and the main reservoir for amino acids. With aging, cachexia, starvation, and myositis, there is a preferential loss of fast glycolytic muscle fibers. We previously reported a mouse model in which a constitutively-active Akt transgene is induced to express in a subset of muscle groups leading to the hypertrophy of type IIb myofibers with an accompanying increase in strength. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

8 Samples

Download data: XLSX