Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

9 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomes of the hybrid mouse diversity panel subjected to Isoproterenol challenge

ABSTRACT: Transcriptomes performed on left ventricular heart samples from mice of the hybrid mouse diversity panel, a set of over a hundred inbred strains of mice. In this project, the strains were challenged with Isoproterenol, a beta-adrenergic agonist to induce cardiac hypertrophy and failure. Results are useful for the analysis of heart-related traits in mice Mice were given three weeks of ISO @ 20ug/g/day for three weeks, then sacrificed. Left ventricles from these mice and matched controls were used for transcripome analysis.

ORGANISM(S): Mus musculus

SUBMITTER: Christoph Rau

PROVIDER: E-GEOD-48760 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Analysis of cardiac gene expression in response to isoproterenol-induced heart failure (part 1)

Project description: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. WT mice developed lung oedema and left ventricular dilatation indicating the development of heart failure. In contrast, myo-/- mice displayed conserved cardiac function and no signs of heart failure. Analysis of the cardiac gene expression profile using 40 k mouse oligonucleotide arrays showed that isoproterenol affected the expression of 180 genes in WT but only 92 genes of myo-/- hearts. Only 40 of these genes were regulated in WT and myo-/- hearts. Whereas in WT hearts a prononced induction of genes of the extracellular matrix occurred suggesting a higher level of remodelling, in myo-/- hearts genes of carbon metabolism and genes linked to inhibition of apoptosis and muscular repair were altered. Interestingly, a subset of genes which was altered in myo-/- mice already under basal conditions was differentially expressed in WT hearts under isoproterenol treatment. In summary, our data show, that the genetic background (WT, myo-/-) has a major impact on cardiac gene expression even in the context of an aggressive hypertrophy model such as chronic isoproterenol stimulation. Keywords: gene expression profiling of isoproterenol induced heart failure in WT and myo-/- mice We analysed the cardiac gene expression profiles in a total of 32 hearts subdivided into 4 groups (8 WT vehicle, 8 WT ISO, 8 myo-/- vehicle, 8 myo-/- ISO).

2010-05-31 | E-GEOD-16243 | biostudies-arrayexpress

Analysis of cardiac gene expression in response to isoproterenol-induced heart failure (part 2)

2010-05-31 | E-GEOD-16246 | biostudies-arrayexpress

Genome-wide gene expression analysis of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice.

Project description:Genome-wide gene expression analysis of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice. These data show that of new CMs derived from resident c-kitpos eCSCs have a gene expression profile that closely resembles the specific gene expression of adult cardiomyocytes. This result supports a role of c-kitpos eCSCs in the regeneration and repair of myocardial damage. To test the identity and the degree of differentiation of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice. Global gene expression profiles by microarray was obtained in c-kitpos eCSCs, c-kitpos eCSC-derived YFPpos CMs and normal adult CMs. c-kitposCD45neg eCSCs were isolated from B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J mice and harvested at 4th passage (n=3). YFPpos cardiomyocytes were FACS sorted from left ventricle apex of Lentirius-c-kit/cre recombined B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J mice 28 days after ISO (N=3). Normal adult CMs were isolated from B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J mice (n=3).

2013-07-30 | E-GEOD-49318 | biostudies-arrayexpress

Transcriptome profiling of left ventricles from cardiac-specific GRK-beta1AR transgenic and/or miR-150 transgenic mice treated with isoproterenol.

Project description:Genome-wide transcriptomic analyses in left ventricles (LVs) from cardiac-specific GRK-beta1AR transgenic (TG) and/or miR-150 TG mice treated with isoproterenol (ISO) were performed to identify novel targets of beta-arrestin-mediated beta1AR signaling and miR-150 in the heart.

2023-01-01 | GSE199195 | GEO

Circular RNA profiling of left ventricles from cardiac-specific GRK-beta1AR transgenic and/or miR-150 transgenic mice treated with isoproterenol.

Project description:Genome-wide circular RNA profiling analyses in left ventricles (LVs) from cardiac-specific GRK-beta1AR transgenic (TG) and/or miR-150 TG mice treated with isoproterenol (ISO) were performed to identify novel circular RNAs regulated by beta-arrestin-mediated beta1AR signaling and miR-150 in the heart.

2023-01-01 | GSE199290 | GEO

Transcription profiling of mouse isoproterenol-induced cardiomyopathy and comparison to exercise-induced cardiac hypertrophy

Project description: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. Experiment Overall Design: Three different sets of mouse hearts were compared: Sedentary mice, mice that were exercised (swimming) for 3 months, and mice that were given isoproterenol via a surgically implanted pump. Each experiment was performed in triplicate - one heart per array. This resulted in a total of 9 arrays.

2009-11-10 | E-GEOD-18801 | biostudies-arrayexpress

Isoproterenol-induced cardiac hypertrophy trigger proteome remodeling of mouse cardiomyocytes

Project description:Cardiac hypertrophy consists in the enlargement of cardiomyocytes and alteration of the extracellular matrix organization in response to physiological or pathological stress. In pathological hypertrophy ocuurs myocardial damage, loss of cardiomyocytes, fibrosis, inflammation, sarcomere disorganization and metabolic impairment, leading to cardiac dysfunction.The rodent model treated with isoproterenol induces cardiac hypertrophy due the constant activation of β-adrenergic receptors. We conducted a quantitative label-free proteomic analysis of cardiomyocytes isolated from hearts of mice treated or not with isoproterenol to better understand the molecular bases of cellular response due to isoproterenol-induced injury.

2020-05-27 | PXD013020 | Pride

Transcriptomes of the hybrid mouse diversity panel subjected to Isoproterenol challenge

Project description:Transcriptomes performed on left ventricular heart samples from mice of the hybrid mouse diversity panel, a set of over a hundred inbred strains of mice. In this project, the strains were challenged with Isoproterenol, a beta-adrenergic agonist to induce cardiac hypertrophy and failure. Results are useful for the analysis of heart-related traits in mice

2013-07-10 | GSE48760 | GEO

Early gene expression in salivary gland after isoproterenol treatment

Project description:Isoproterenol, a Î²-adrenergic agonist, has been shown to induce salivary gland hyperplasia. To gain a better understanding of the underlying molecular changes altered by isoproterenol, microarray-based gene expression analysis was conducted on rat parotid glands at 10, 30, and 60 minutes after isoproterenol injection. After isoproterenol treatment, the number of differentially expressed genes was increased in a time-dependent manner. The regulation of up- and down-expression of genes related to cell proliferation/survival provides a better understanding of the mechanism of isoproterenol-induced parotid gland enlargement. For the time-course experiments, male Sprague-Dawley rats (2-3 months old) were injected intra-peritoneally with isoproterenol (20 mg/g body weight) or normal saline (control). The rats were euthanized at the indicated times and the harvested parotid glands stored at -80C until analyzed. Cells were harvested and processed at the following times: control (saline), immediately after treatment (10 min) and at 30 and 60min after treatment.

2015-03-01 | E-GEOD-54965 | biostudies-arrayexpress

Set7 deletion attenuates isoproterenol-induced cardiac fibrosis and prevents heart failure

Project description:The Set7 methyltransferase regulates the expression of several genes through the methylation of histones and modulates the activity of non-histone proteins. However, the role of Set7 in cardiac remodeling and heart failure remains unknown. To address this question, wild type (WT) and Set7 knockout (KO) male mice were injected with isoproterenol (60 mg/kg) or saline subcutaneously for 14 days. WT mice injected with isoproterenol displayed a decrease in Set7 activity in the heart, although Set7 protein levels were unchanged. WT and Set7 KO mice injected with isoproterenol exhibited an increase in the heart weight and cardiomyocyte area compared to their respective controls. However, Set7 KO mice displayed an exacerbated cardiac hypertrophy in response to isoproterenol compared to WT mice. In addition, Set7 deletion attenuated isoproterenol-induced cardiac fibrosis. Echocardiograms revealed that WT mice injected with isoproterenol had lowered ejection fractions and fractional shortening, and increased E/A ratios compared to their controls. Conversely, Set7 KO mice did not show alteration in these parameters in response to isoproterenol. Both isoproterenol and Set7 deletion changed the transcriptional profile of the heart. Moreover, Set7 deletion increased the expression of mitochondrial biogenesis and antioxidant factors in the heart and reduced the expression of cellular senescence and inflammation markers. Taken together, our data suggest that Set7 deletion reduces isoproterenol-induced myocardial fibrosis and prevents heart failure, suggesting that Set7 plays an important role in cardiac remodeling and function.

2024-04-18 | GSE207581 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data