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E-GEOD-77

ABSTRACT: Transcription profiling of heart ventricles from mice that have cardiac hypertrophy induced by swimming training

PROVIDER: E-GEOD-77 | ExpressionAtlas | 2015-10-22

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-77-analysis-methods.tsv	Tabular
	E-GEOD-77-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-77-configuration.xml	Xml
	E-GEOD-77-percentile-ranks.tsv	Tabular
	E-GEOD-77.condensed-sdrf.tsv	Tabular

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E-GEOD-76

Project description:Transcription profiling of heart ventricles from mice at different time points after surgical intervention for pressure-overload induced hypertrophy to identify differentially expressed genes.

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Gene and exon expression change in cardiac hypertrophy with pressure overload

Project description:Pathological cardiac hypertrophy was induced by pressure overload on the heart. We performed genome-wide exon array experiments with left ventricles of mice with 1 week and 4 week of transverse aortic constriction (TAC). The exon level analysis revealed widespread regulation of alternative splicing and alternative polyadenylation during hypertrophy. Exon and gene expression changes were examined in 1 week and 4 week TAC-operated hearts compared to sham-operated hearts. We used C57/BL6 wildtype mice, and their left ventricles were subject to surgery (each n=2).

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E-GEOD-2507

Project description:Transcription profiling by array of skeletal and cardiac muscle from dysferlin-deficient mice

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Transcription profiling of hearts from mice heterozygous for Gata4 mutation (G4D) to investigate the significance of Gata4 in regulating postnatal heart function and in regulating the hypertrophic response of the heart to pathological stress.

Project description: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. To test this hypothesis, we studied mice heterozygous for deletion of the second exon of Gata4 (G4D). At baseline, G4D mice had mild systolic and diastolic dysfunction associated with reduced heart weight and decreased cardiomyocyte number. After transverse aortic constriction (TAC), G4D mice developed overt heart failure and eccentric cardiac hypertrophy, associated with significantly increased fibrosis and cardiomyocyte apoptosis. Inhibition of apoptosis by overexpression of the insulin-like growth factor 1 receptor prevented TAC-induced heart failure in G4D mice. Unlike WT-TAC controls, G4D-TAC cardiomyocytes hypertrophied by increasing in length more than width. Gene expression profiling revealed upregulation of genes associated with apoptosis and fibrosis, including members of the TGF? pathway. Our data demonstrate that Gata4 is essential for cardiac function in the postnatal heart. After pressure overload, Gata4 regulates the pattern of cardiomyocyte hypertrophy and protects the heart from load-induced failure. Experiment Overall Design: We reasoned that if Gata4 was a crucial regulator of pathways necessary for cardiac hypertrophy, then modest reductions of Gata4 activity should result in an observable cardiac phenotype. To test this hypothesis, we used gene targeted mice that express reduced levels of Gata4. We characterized these mice at baseline and after pressure Experiment Overall Design: overload.

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E-GEOD-63848

Project description:Transcription profiling by array of cardic ventricle tissues from mice with cardiac-specific constitutive expression of an activated Akt (caAkt) and wild-type controls to test whether Akt activation contributes to mitochondrial dysfunction in pathological cardiac hypertrophy

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