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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.

ABSTRACT: 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

ORGANISM(S): Mus musculus

SUBMITTER: Martina Schinke

PROVIDER: E-GEOD-76 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

2002-07-30 | GSE76 | GEO

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

Exercised Induced Hypertrophy

2002-08-02 | GSE77 | GEO

CHF1/Hey2 Promotes Physiological Hypertrophy in response to Pressure Overload

Project description:We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy. To determine the role of CHF1/Hey2 in pressure overload hypertrophy, we performed ascending aortic banding on wild type and transgenic mice overexpressing CHF1/Hey2 in the myocardium. We found that both wild type and transgenic mice developed increased ventricular weight to body weight ratios one week after aortic banding. Wild type mice also developed decreased fractional shortening after one week when compared to preoperative echocardiograms and sham operated controls. Transgenic mice, in comparison, demonstrated preserved fractional shortening. Histological examination of explanted heart tissue demonstrated extensive fibrosis in wild type hearts, but minimal fibrosis in transgenic hearts. TUNEL staining demonstrated increased apoptosis in the wild type hearts but not in the transgenic hearts. Exposure of cultured neonatal myocytes from wild type and transgenic animals to hydrogen peroxide, a potent inducer of apoptosis, demonstrated increased apoptosis in the wild type cells. Gene Set Analysis of microarray data from wild type and transgenic hearts one week after banding revealed suppression and activation of multiple pathways involving apoptosis, cell signaling and biosynthesis. These findings demonstrate that CHF1/Hey2 promotes physiological over pathological hypertrophy in pressure overload through suppression of apoptosis and global regulation of multiple transcriptional pathways.

2010-01-20 | GSE13031 | 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

The calcineurin splicing variant CnAb1 reduces pressure overload-induced cardiac hypertrophy by promoting mitohormesis

Project description:Analysis of the function of CnAb1 in myocardial hypertrophy in mice using a Gain of Function strategy and Trans Aortic Banding as a hypertrophic stimuly. Microarray was performed after QPCR validation of the upregulation of CnAb1.

2019-03-01 | GSE79536 | GEO

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

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

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

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

Pimobendan attenuates pressure overload-induced myocardial hypertrophy by inhibiting the MAPKs pathway

Project description:Background: Although myocardial hypertrophy is an essential component of heart’s response to many forms of stress, prolonger excessive hypertrophy contributes importantly to the pathogenesis of heart disease. The pimobendan is a drug that both inhibits phosphodiesterase 3 (PDE3) and acts as a calcium sensitizer, which has been used to treat heart failure. The effects of pimobendan on myocardial hypertrophy is controversial. Objective: This study aims to evaluate the therapeutic effect of pimobendan on myocardial hypertrophy. Methods: Mice were treated with low oral doses of pimobendan (1mg/kg/d) for 4 weeks after transaortic constriction. Heart structure and function was assessed using ultrasound, hemodynamic measurements and histology combined with biochemical assessments of myocardial hypertrophy. We also examined the effects of pimobendan (100 µM) on hypertrophy in cultured neonatal rat cardiomyocytes (NRCMs) induced by 50 µM phenylephrine (PE). Results: The doses pimobendan used in our studies had no effect on baseline contractility. Nevertheless, pimobendan administration of mice subjected to TAC decreased heart weights (normalized to either tibia length or body weight) ventricular wall thickness, cardiomyocyte sizes, myocardial fibrosis and the levels of a number of key myocardial hypertrophy markers (WHICH ONES). In cultured neonatal cardiomyocytes, pimobendan attenuated the PE-induced hypertrophy. In both hypertrophy models pimobendan reduced the phosphorylation levels of several essential proteins in the MAPK pathway, PI3K-AKT pathway, and calcineurin signaling pathway. Conclusion: Low pimobendan may attenuate myocardial hypertrophy. Although the underlying mechanisms remain to be elucidated, the MAPK pathway is likely to play a role.

2023-07-01 | GSE182501 | 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

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