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Exercised Induced Hypertrophy

ABSTRACT: The Affymetrix GeneChip MgU74Av2 was used to analyze expression profiles of mice that had cardiac hypertrophy induced by swimming training. More information of this model can be obtained at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/swim_home.html Keywords = exercise induced hypertrophy, cardiac Keywords: time-course

ORGANISM(S): Mus musculus

PROVIDER: GSE77 | GEO | 2002/08/02

SECONDARY ACCESSION(S): PRJNA85513

REPOSITORIES: GEO

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Transcription profiling of heart ventricles from mice that have cardiac hypertrophy induced by swimming training to study the molecular mechanism of exercise induced hypertrophy.

Project description:The Affymetrix GeneChip MgU74Av2 was used to analyze expression profiles of mice that had cardiac hypertrophy induced by swimming training. More information of this model can be obtained at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/swim_home.html

2007-12-19 | E-GEOD-77 | biostudies-arrayexpress

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

2002-07-30 | GSE76 | GEO

Physiologic cardiac hypertrophy

Project description:Dahl salt-sensitive (DS) rats were obtained from Harlan Sprague Dawley Laboratory at 5 weeks of age. At 6 weeks of age, physiologic cardiac hypertrophy was generated by a vigorous daily exercise regimen for 6 weeks (e group). The exercise protocol is based on those described previously with modifications (Wisloff U et al., 2001; Jin H et al., 1994). Rats were exercised daily for 6 weeks on a rodent treadmill (Exer-6M; Columbus Instruments). The exercise program consisted of three weeks of progressively strenuous exercise regimens; followed by three weeks of maintenance period, during which the rats were exercised at 16 m/min at a 5o incline for 90 minutes/day. All rats completed the exercise protocol. Pathological cardiac hypertrophy was generated by feeding a 6% NaCl diet to DS rats at 6 weeks of age (h group) (Inoko M et al., 1994). Control rats (c group) were age matched and sedentary DS rats fed normal rat chow. Read more at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/rat_home.html Keywords: other

2003-10-24 | GSE776 | GEO

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

FVB Benchmark Set for Cardiac Development, Maturation, and Aging

Project description:The Affymetrix GeneChip MgU74Av1 was used to analyze expression profiles of mice at different developmental stages to monitor changes in cardiac gene expression over time. More information about this model may be obtained at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/fvb_home.html Keywords = Cardiac development Keywords: time-course

2002-07-30 | GSE75 | GEO

Transcription profiling of rat heart samples from animals with physiological or pathological cardiac hypertrophy

Project description:Dahl salt-sensitive (DS) rats were obtained from Harlan Sprague Dawley Laboratory at 5 weeks of age. At 6 weeks of age, physiologic cardiac hypertrophy was generated by a; vigorous daily exercise regimen for 6 weeks (e group). The exercise protocol is based on those described previously with modifications (Wisloff U et al., 2001; Jin H et al., 1994). Rats were exercised daily for 6 weeks on a rodent treadmill (Exer-6M; Columbus Instruments). The exercise program consisted of three weeks of progressively strenuous exercise regimens; followed by three weeks of maintenance period, during which the rats were exercised at 16 m/min at a 5o incline for 90 minutes/day. All rats completed the exercise protocol. Pathological cardiac hypertrophy was generated by feeding a 6% NaCl diet to DS rats at 6 weeks of age (h group) (Inoko M et al., 1994). Control rats (c group) were age matched and sedentary DS rats fed normal rat chow. Read more at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/rat_home.html<br><br>Note that files GSM11886.txt and GSM12308.txt, and files GSM11887.txt and GSM12309.txt as downloaded from GEO contain identical data.

2007-10-11 | E-GEOD-776 | biostudies-arrayexpress

Transcriptome analysis of mouse cardiac hypertrophy

Project description:RNA-Seq analysis of mouse cardiac transcriptome. Transverse aortic contraction was used to induce cardiac hypertrophy (TAC). To compare wild type and physiological cardiac hypertrophy 'Sendetary' (feeding mouse during 4 weeks) and 'Swim (exercise training to induce the cardiac hypertrophy) samples were analysed.

2012-05-11 | E-MTAB-727 | biostudies-arrayexpress

Gene profiling of pathological cardiac hypertrophy vs physiological hypertrophy

Project description:Cardiac hypertrophy can lead to heart failure, and is induced either by physiological stimuli eg postnatal development, chronic exercise training or pathological stimuli eg pressure or volume overload. Majority of new therapies for heart failure has mixed outcomes. A combined mouse model and oligo-array approach are used to examine whether phosphoinositide 3-kinase (p110-alpha isoform) activity is critical for maintenance of cardiac function and long-term survival in a setting of heart failure. The significance and expected outcome are to recognise genes involved in models of heart failure ie pathological- vs physiology-hypertrophy, and examine the molecular mechanisms responsible for such activity. Growth of the heart can be induced by physiological stimuli e.g., postnatal development, chronic exercise training, or pathological stimuli e.g., pressure or volume overload. Physiological hypertrophy (“good”) is characterised by a normal organisation of cardiac structure, and normal or enhanced cardiac function. In comparison, pathological hypertrophy (”bad”) is associated with fibrosis, cardiac dysfunction, and increased morbidity and mortality. The mechanistic process which allows the heart to enlarge in response to physiological stimuli while maintaining normal or enhanced function is of great clinical relevance because one potential therapeutic strategy is to inhibit the pathological growth process while augmenting the physiological growth process. One of the major process that regulate heart size is by phosphoinositide 3-kinase (PI3K). Thus the end goal of this project is to determine whether the p110 alpha isoform of PI3K could be a potential tool for augmenting physiological growth and improving cardiac function of the failing diseased heart, and to examine the underlying mechanisms responsible. Keywords: Disease progression analysis

2010-03-08 | GSE7487 | GEO

Transcription profiling of heart ventricles from mice at different developmental stages to monitor changes in cardiac gene expression over time.

2007-12-15 | E-GEOD-75 | biostudies-arrayexpress

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

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