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E-GEOD-76

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

PROVIDER: E-GEOD-76 | ExpressionAtlas | 2015-10-22

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-76-analysis-methods.tsv	Tabular
	E-GEOD-76-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-76-configuration.xml	Xml
	E-GEOD-76-percentile-ranks.tsv	Tabular
	E-GEOD-76.condensed-sdrf.tsv	Tabular

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Pressure-Overload Induced Cardiac Hypertrophy

Project description:Aortic banding is an excellent model system to evaluate the process of development of left ventricular hypertrophy in response to hemodynamic stress. The Affymetrix GeneChip MgU74Av1 was used to analyze expression profiles of mice at different time points after surgical intervention for pressure-overload induced hypertrophy. More information about this model may be obtained at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/band_home.html Keywords = Pressure overload, cardiac hypertrophy Keywords: time-course

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Project description:Expression profiles at various time points after surgical intervention for pressure-overload induced cardiac hypertrophy and failure.

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

2007-12-19 | E-GEOD-76 | biostudies-arrayexpress

RNA-seq transcriptonal profiling in mouse hearts under pressure overload

Project description:Heart failure is a leading cause of death in US. Hypertension is one of the most important risk factor of heart failure. In the presence of high blood pressure, the heart manifests hypertrophic growth to ameliorate ventricular wall stress. This once adaptive response may progress into decompensation and heart failure. The precise mechanisms governing this transition remain elusive. Here, we take advantage of mouse surgical model transverce aortic constriction (TAC) to induce pressure overload in rodents. We harvest hearts at different time points post surgery and subject these samples for RNA-Seq analysis with an aim to identify early players in the process and elucidate the molecular mechanisms.

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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-9996

Project description:Transcription profiling by array of Arabidopsis root sections at different time points after cutting

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E-GEOD-4675

Project description:Transcription profiling by array of mouse pre-frontal cortex at different time-points after birth

2014-10-10 | E-GEOD-4675 | ExpressionAtlas

BMPER regulates cardiomyocyte size and vessel density in vivo

Project description:Background: BMPER, an orthologue of Drosophila melanogaster crossveinless-2, is a secreted factor that regulates BMP activity in endothelial cell precursors and during early cardiomyocyte differentiation. Although previously described in the heart, the role of Bmper in cardiac development and function remained unknown. Methods: BMPER deficient hearts were phenotyped histologically and functionally using echocardiography and Doppler analysis. Since BMPER -/- mice die perinatally, BMPER +/- mice were then challenged to pressure overload induced cardiac hypertrophy and hind limb ischemia to determine changes in angiogensis and regulation of cardiomyocyte size. Results: We identified for the first time the cardiac phenotype associated with BMPER haploinsufficiency. BMPER mRNA and protein are present in the heart during cardiac development through at least E14.5 but is lost by E18.5. BMPER +/- ventricles are thinner and less compact than sibling wild-type hearts. In the adult, BMPER +/- hearts present with decreased anterior and posterior wall thickness, decreased cardiomyocyte size, and an increase in cardiac vessel density. Despite these changes, BMPER +/- mice respond to pressure overload-induced cardiac hypertrophy challenge largely to the same extent as wild-type mice. Conclusion: BMPER appears to play a role in regulating both vessel density and cardiac development in vivo; however, BMPER haploinsufficiency does not result in marked effects on cardiac function or adaptation to pressure overload hypertrophy. Unpaired, two-condition experiment, wild-type vs BMPER+/- adult hearts. Biological replicates: 4 per condition.

2012-09-20 | E-GEOD-40983 | biostudies-arrayexpress

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