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Exercise induced cardiac hypertrophy

ABSTRACT: Cardiac hypertrophy was induced by treadmill running. Sedentary animals served as controls. Gene expression was determined by Affymetrix RGU34A GeneChip's to identify genes with differential expression in an adaptive model of cardiac hypertrophy. Keywords: other

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE739 | GEO | 2004/07/12

SECONDARY ACCESSION(S): PRJNA87691

REPOSITORIES: GEO

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Transcription profiling of rat heart samples from active and sedentary animals

Project description:Cardiac hypertrophy was induced by treadmill running. Sedentary animals served as controls. Gene expression was determined by Affymetrix RGU34A GeneChip's to identify genes with differential expression in an adaptive model of cardiac hypertrophy.

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Comparison of exercise and pregnancy-induced cardiac hypertrophy

Project description:Comparative analysis of mouse cardiac left ventricle gene expression: voluntary wheel exercise and pregnancy-induced cardiac hypertrophy We performed microarray analysis on RNA from left ventricles of mice in non-pregnant diestrus cycle, mid-pregnancy (MP), late-pregnancy (LP), and immediate post-partum (0PP). These were compared to 7days (7EX) and 21 days (21EX) of voluntary wheel running exercise.

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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.

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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 tissue from rats that have undergone treadmill exercise or have been sedentary for different lengths of time

Project description:Seventy two rats were randomized to twelve independent groups of rats (n = 6 in all groups) where half of the rats were chosen for training (treadmill exercise training 1.5 hour 5 days a week, in 1, 4, 24, 48 days and for 4 and 8 weeks) or sedentary (no training) as described in detail by Wisloff et al. (Intensity-controlled treadmill running in rats: VO(2 max) and cardiac hypertrophy. Am J Physiol Heart Circ Physiol. 2001 Mar;280(3):H1301-10.) or Kemi et al.(Aerobic fitness is associated with cardiomyocyte contractile capacity and endothelial function in exercise training and detraining. Circulation. 2004 Jun 15;109(23):2897-904. Epub 2004 Jun 1.). The rats were scarified one hour after training (1, 4, 24 and 48 days) or 24 hours after training (4 and 8 weeks). Biopsies form left ventricle was taken form all rats and stored on -80°C for preparation of RNA. The same procedures were performed for the control/sedentary rats which were sacrificed at the same time as the exercised rats.

2006-11-10 | E-TABM-166 | biostudies-arrayexpress

Transcription profiling of rat heart left ventricle after exercise to investigate the role of exercise as a known protective factor against cardiovascular morbidity and mortality

Project description:Physical exercise training is a known protective factor against cardiovascular morbidity and mortality. Nevertheless, the underlying specific molecular mechanisms still remain uncompletely explored. To identify molecular mechanisms by which exercise training induces this favorable phenotype a genomic approach was used in an animal model of mild exercise previously demonstrated by our group to induce cardioprotection. Our data indicate that mild exercise by inducing no or few permanent changes in gene expression profile is able to determine cardioprotection without induction of cardiac hypertrophy. Experiment Overall Design: We investigated the gene expression profile by Affymetrix technology (230 2.0 GeneChip rat genome array) induced by mild exercise training (treadmill running: 25 m/min, 10% incline, 1 h/day, 3 days/week, 10 weeks) on left ventricle (LV) of exercise-trained (n=10) and sedentary control (n=10) rats.

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miRNA-99 family diverges physiological cardiac hypertrophy to pathological cardiac hypertrophy

Project description:Purpose: The physiological cardiac hypertrophy is an adaptive condition that does not associate with myocyte cell death while pathological hypertrophy is a maladaptive condition associated with myocyte cell death. Alpha-2 macroglobulin (Î±-2M) an acute phase protein induces cardiac hypertrophy via the ERK1,2 and PI3K/Akt signaling. This study is aimed at exploring the miRNome of Î±-2M induced hypertrophied cardiomyocytes and to understand the role of miRNAs in determination of pathological and physiological hypertrophy. Methods: Hypertrophy was induced in H9c2 cardiomyoblasts using alpha-2 macroglobulin. The induction of hypertrophy is confirmed by microscopy and gene expression studies. Subsequently, the total RNA was isolated and small RNA sequencing was executed in Illumina HiSeq 2000. Results: Analysis of small RNA reads revealed the differential expression of a large set of miRNAs during hypertrophy. Among the differentially expressed candidates, miR-99 family (miR-99a, miR-99b and miR-100) showed significant downregulation upon Î±-2M treatment while isoproterenol treatment (pathological hypertrophy) upregulated their expression. The binding site for Egr1 transcription factor was identified in the promoter region of miR-99 family, and interestingly all miRNAs with Egr1 binding site proven by ChIP-Seq were downregulated during physiological hypertrophy Conclusions: The results proved Egr-1 mediated regulation of miR-99 family determines the uniqueness of pathological and physiological hypertrophy. Upregulated miR-99 expression during pathological hypertrophy suggests that it can be a valuable diagnostic marker and potential therapeutic target for cardiac hypertrophy and heart failure. Small RNA profiles of control and hypertrophied cardiomyocyte H9c2 cells were generated by deep sequencing using Illumina HiSeq 2000

2015-11-01 | E-GEOD-73597 | biostudies-arrayexpress

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

Rat models of cardiac hypertrophy

Project description:Cardiac hypertrophy was induced by aortic banding (6, 12, 16, and 30 weeks), myocardial infarction (3 and 9 weeks), an av-fistula (aorta abd. to v. cava inf.. 3 and 8 weeks), or hormone infusion (two weeks either angiotensin 2 or a thyroxin analogue). Sham operated or saline infused animals served as controls. Gene expression was determined by Affymetrix RGU34A GeneChip's to identify genes with common regulation in the different models of cardiac hypertrophy. Keywords: other

2004-03-12 | GSE738 | GEO

Comparison of exercise and pregnancy-induced cardiac hypertrophy

Project description:Comparative analysis of mouse cardiac left ventricle gene expression: voluntary wheel exercise and pregnancy-induced cardiac hypertrophy

2012-03-08 | GSE36330 | GEO

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