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E-GEOD-760

ABSTRACT: Transcription profiling of heart ventricles from 10 week old mice heterozygous for dn-p21ras and 3 month old wild type FVB mice to study severe dilated cardiomyopathy.

PROVIDER: E-GEOD-760 | ExpressionAtlas | 2015-10-13

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-760-analysis-methods.tsv	Tabular
	E-GEOD-760-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-760-configuration.xml	Xml
	E-GEOD-760-percentile-ranks.tsv	Tabular
	E-GEOD-760.condensed-sdrf.tsv	Tabular

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Overexpression of dn-p21ras as a model system for severe dilated cardiomyopathy

Project description:Mice heterozygous for dn-p21 littermates were sacrificed at 10 weeks of age. Ventricles were isolated and snap-frozen in liquid nitrogen. Use 3 month old FVB Females as controls. [GSM2334, GSM2335, GSM2336] Read more at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/ras_home.html Keywords = ras Keywords = dilated cardiomyopathy Keywords: other

2003-10-24 | GSE760 | GEO

Transcription profiling of heart ventricles from 10 week old mice heterozygous for dn-p21ras and 3 month old wild type FVB mice to study severe dilated cardiomyopathy.

Project description:Mice heterozygous for dn-p21 littermates were sacrificed at 10 weeks of age. Ventricles were isolated and snap-frozen in liquid nitrogen. Use 3 month old FVB Females as controls. [GSM2334, GSM2335, GSM2336]; Read more at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/ras_home.html

2007-12-15 | E-GEOD-760 | biostudies-arrayexpress

CTCF point mutation at R567 disrupts mouse heart development via 3D genome rearrangement and transcription dysregulation [RNA-seq]

Project description:In this study, we analyzed gene expression change in heart tissues from 8-week-old wild-type and Ctcf heterozygous mutant mice by using RNA-seq.

2025-04-09 | GSE276744 | GEO

Migraine-associated mutation in the Na,K-ATPase leads to disturbances in cardiac metabolism and reduced cardiac function

Project description:Background. Mutations in ATP1A2 gene encoding the Na,K-ATPase α2 isoform is associated with familial hemiplegic migraine type 2 (FHM2). Migraine with aura is a known risk factor for heart disease. The Na,K-ATPase is important for cardiac function but its role for heart disease remains unknown. We hypothesized that ATP1A2 is a susceptibility gene for heart disease and aimed to assess the underlying disease mechanism. Methods and Results. Mice heterozygous for the FHM2-associated G301R mutation in the Atp1a2 gene (α2+/G301R mice) and matching wild type (WT) controls were compared. Reduced expression of the Na,K-ATPase α2 isoform and increased expression of the α1 isoform was observed in hearts from α2+/G301R mice (Western blot). Left ventricular dilation and reduced ejection fraction was shown in hearts from 8-month-old α2+/G301R mice (cardiac magnetic resonance imaging) and this was associated with reduced nocturnal blood pressure (radiotelemetry). Cardiac function and blood pressure of 3-month-old α2+/G301R mice were similar to WT mice. Amplified Na,K-ATPase-dependent Src/Ras/Erk1/2 signaling was observed in hearts from 8-month-old α2+/G301R mice and this was associated with mitochondrial uncoupling (respirometry), increased oxidative stress (malonedialdehyde measurements), and a heart failure-associated metabolic shift (hyperpolarized magnetic resonance). Mitochondrial membrane potential was similar between the groups (JC-1 dye assay). Proteomics of heart tissue further suggested amplified Src/Ras/Erk1/2 signaling and increased oxidative stress and provided the molecular basis for systolic dysfunction in 8-month-old α2+/G301R mice. Conclusions. Our findings suggest that ATP1A2 mutation leads to disturbed cardiac metabolism and reduced cardiac function mediated via Na,K-ATPase-dependent ROS signaling through the Src/Ras/Erk1/2 pathway.

2022-05-20 | PXD028952 | Pride

MicroRNA-34a regulates cardiac ageing and function

Project description:We compared the heart of 6-weeks-old mice (young) with 18-months-old mice (old) hearts of 6 week old and 18 month old mice

2013-02-20 | E-GEOD-43556 | biostudies-arrayexpress

Microarray gene expression profiling of cardiac genes at the onset of heart failure

Project description:Atherosclerosis and pressure overload are major risk factors for the development of heart failure in patients. Cardiac hypertrophy often precedes the development of heart failure. However, underlying mechanisms are incompletely understood. To investigate pathomechanisms underlying the transition from cardiac hypertrophy to heart failure we used experimental models of atherosclerosis- and pressure overload-induced cardiac hypertrophy and failure, i.e. apolipoprotein E (apoE)-deficient mice, which develop heart failure at an age of 18 months, and non-transgenic C57BL/6J (B6) mice with heart failure triggered by 6 months of pressure overload induced by abdominal aortic constriction (AAC). The development of heart failure was monitored by echocardiography, invasive hemodynamics and histology. The microarray gene expression study of cardiac genes was performed with heart tissue from failing hearts relative to hypertrophic and healthy heart tissue, respectively. The microarray study revealed that the onset of heart failure was accompanied by a strong up-regulation of cardiac lipid metabolism genes involved in fat synthesis, storage and oxidation. Microarray gene expression profiling was performed with heart tissue isolated from (i) 18 month-old apoE-deficient mice relative to age-matched non-transgenic C57BL/6J (B6) mice, (ii) 6 month-old apoE-deficient mice with 2 months of chronic pressure overload induced by abdominal aortic constriction (AAC) relative to sham-operated apoE-deficient mice and nontransgenic B6 mice, (iii) 10 month-old B6 mice with 6 months of AAC relative to sham-operated B6 mice, and (iv) 5 month-old B6 mice with 1 month of AAC relative to age-matched B6 mice.

2010-12-03 | E-GEOD-25765 | biostudies-arrayexpress

RT quantitative PCR analysis of inflammasome related genes in mice choclea after noise exposure

Project description:Six month-old wild type and Igf1 heterozygous mice were exposed to a violet swept sine noise (frequency range 2–20 kHz) at 110 dB SPL for 30 minutes. Cochlear samples were taken at 2 and 24 hours post-noise exposure to study the evolution of the expression of inflammation genes by using PCR arrays and RT-qPCR. Six month-old wild type and Igf1 heterozygous mice not exposed to noise were used as control.

2017-11-09 | GSE106667 | GEO

RT quantitative PCR analysis of p53 Signaling Pathway related genes in mice choclea after noise exposure.

2018-06-30 | GSE116460 | GEO

GRK2 deficiency confers cardioprotective profile.

Project description:This SuperSeries is composed of the following subset Series: GSE41706: Expression data from adult (9 month-old) hearts from GRK2 heterozygous C57BL/6J mice and its wild type littermates GSE41807: Expression data from adult (9 month-old) and young (4 month-old) hearts from C57BL/6J mice GSE41808: Expression data from adult (9 month-old) and young (4 month-old) hearts from GRK2 heterozygous C57BL/6J mice. GSE41809: Expression data from young (4 month-old) hearts from GRK2 heterozygous C57BL/6J mice and its wild type littermates Refer to individual Series

2012-10-25 | E-GEOD-41810 | biostudies-arrayexpress

Expression data of MCK conditional frataxin knock-out mice

Project description:Frataxin deficiency in human is the cause of Friedreich's ataxia (FA), a lethal neuro- and cardio-degenerative disease. Knock-out (KO) mice of this mouse model of FA exhibit classical cardiomyopathy of the patients. The onset of FA phenotypes in the KO mice is approximately 6-7 weeks of age. This genearray analysis was conducted to examine the changes in gene expression in the heart of KO mice relative to their wild-type (WT) littermates at 4- and 10-weeks of age. At 10-weeks of age, the KO mice begin to die from severe cardiomyopathy. RNA from the heart of four female 4-week-old MCK littermates (two WT and two KO) and four female 10-week-old MCK littermates (two WT and two KO) was extracted and hybridised to Affymetrix Mouse Genome 430 2.0 Array.

2011-12-31 | E-GEOD-31208 | biostudies-arrayexpress

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