Cardiac left ventricular physiological hypertrophy in swine
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ABSTRACT:
ORGANISM(S): Sus scrofa
PROVIDER: GSE37922 | GEO | 2014/06/01
SECONDARY ACCESSION(S): PRJNA165671
REPOSITORIES: GEO
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Project description:The molecular mechanism underlying cardiac remodeling following exercise have been incompletely understood. Until now, most studies have been performed in rodents. We studied cardiac remodeling in the physiologically more relevant animal model, the swine. Microarray analysis was performed on animals that underwent either and exercise protocol or remained sedentary. RNA was isolated from tissue samples from the endocardial layer of the free wall of the left ventricle. RNA was isolated from 8 exercise-trained and 8 sedentary animals 4-5 weeks after start of the protocol. Each group contained 4 males and 4 females. Animals used for the study were 2-3 months old Yorkshire x Landrace swine. Only neutered males entered the study.
2014-06-01 | E-GEOD-37922 | biostudies-arrayexpress
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
Project description:BACKGROUND - MicroRNAs (miRs) are a class of small non-coding RNAs that regulate gene expression. Transgenic models have proved that a single miR can induce pathological cardiac hypertrophy and failure. The roles of miRs in the genesis of physiologic left ventricular hypertrophy (LVH), however, are not well elucidated. OBJECTIVE - To evaluate miRs expression in an experimental model of exercise-induced LVH. METHODS - Male Balb/c mice were divided into sedentary (SED) and exercise (EXE) groups. Voluntary exercise was performed in odometer-monitored metal wheels during 35 days. Analyses were performed after 7 and 35 days of training, and consisted of transthoracic echocardiography, maximal exercise test, miRs microarray (miRBase v.16) and real-time qRT-PCR analysis. RESULTS - Left ventricular weight/body weight ratio increased by 7% in the EXE group at day 7 (p<0.01) and by 11% at 35 days of training (p<0.001) After 7 days of training, microarray identified 35 deregulated miRs: 20 had an increase in their expression and 15 were down-regulated (p=0.01). At day 35 of training, 25 miRs were deregulated: 15 were up-regulated and 10 had decreased their expression compared to the SED group (p<0.01). qRT-PCR confirmed an increase in miR-150 levels at both time points and a decrease in miR-26b, miR-27a and miR-143 after 7 days of voluntary exercise. CONCLUSIONS M-bM-^@M-^S We unraveled new miRs that can modulate physiological cardiac hypertrophy, particularly miR-26b, -150, 27a and -143. Our data also indicate that previously established regulatory gene pathways involved in pathological LVH are not deregulated in physiologic LVH. Experimental model of left ventricular hypertrophy induced by voluntary exercise Male Balb/c mice, 8-10 weeks old, 4 groups analyzed, each group consisted of a pool from 4 animals
2014-06-01 | E-GEOD-52278 | biostudies-arrayexpress
Project description:The molecular mechanism underlying cardiac remodeling following myocardial infarction have been incompletely understood. Until now, most studies have been performed in rodents. We studied cardiac remodeling in the physiologically more relevant animal model, the swine. Microarray analysis was performed on animals that underwent either sham surgery or permanent ligation of the left coronary artery (MI). RNA was isolated from the remote, non-ischemic, regions of the left ventricle. RNA was isolated from 8 sham and 8 MI animals three weeks after surgery. Each group contained 4 males and 4 females. Animals used for the study were 2-3 months old Yorkshire x Landrace swine. Only neutered males entered the study.
2011-12-21 | E-GEOD-27962 | biostudies-arrayexpress
Project description:BACKGROUND - MicroRNAs (miRs) are a class of small non-coding RNAs that regulate gene expression. Transgenic models have proved that a single miR can induce pathological cardiac hypertrophy and failure. The roles of miRs in the genesis of physiologic left ventricular hypertrophy (LVH), however, are not well elucidated. OBJECTIVE - To evaluate miRs expression in an experimental model of exercise-induced LVH. METHODS - Male Balb/c mice were divided into sedentary (SED) and exercise (EXE) groups. Voluntary exercise was performed in odometer-monitored metal wheels during 35 days. Analyses were performed after 7 and 35 days of training, and consisted of transthoracic echocardiography, maximal exercise test, miRs microarray (miRBase v.16) and real-time qRT-PCR analysis. RESULTS - Left ventricular weight/body weight ratio increased by 7% in the EXE group at day 7 (p<0.01) and by 11% at 35 days of training (p<0.001) After 7 days of training, microarray identified 35 deregulated miRs: 20 had an increase in their expression and 15 were down-regulated (p=0.01). At day 35 of training, 25 miRs were deregulated: 15 were up-regulated and 10 had decreased their expression compared to the SED group (p<0.01). qRT-PCR confirmed an increase in miR-150 levels at both time points and a decrease in miR-26b, miR-27a and miR-143 after 7 days of voluntary exercise. CONCLUSIONS – We unraveled new miRs that can modulate physiological cardiac hypertrophy, particularly miR-26b, -150, 27a and -143. Our data also indicate that previously established regulatory gene pathways involved in pathological LVH are not deregulated in physiologic LVH.
2014-06-01 | GSE52278 | GEO
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
Project description:Background: Exercise can induce physiological myocardial hypertrophy (PMH), and former athletes can live 5-6 years longer than nonathletic controls, suggesting a benefit after regression of PMH. We previously reported that regression of pathological myocardial hypertrophy has antihypertrophic effects. Accordingly, we hypothesized that antihypertrophic memory exists even after PMH has regressed, increasing myocardial resistance to subsequent pathological hypertrophic stress. Methods and Results: C57BL/6 mice were submitted to 21 days of swimming training to develop PMH. After termination of exercise, PMH regressed within 1 week. PMH regression mice (hypertrophic preconditioning group, EHP) and sedentary mice (control group) then underwent transverse aortic constriction (TAC) or a sham operation. At 1 and 4 weeks after TAC, the EHP group showed less increase in myocardial hypertrophy and lower expression of the Nppa and Myh7 genes than the sedentary group. At 4 weeks after TAC, EHP mice had less pulmonary congestion, smaller left ventricular dimensions and end-diastolic pressure, and a larger left ventricular ejection fraction and maximum pressure change rate than sedentary mice. Quantitative polymerase chain reaction (qPCR) revealed that the long noncoding myosin heavy chain associated RNA transcript Mhrt779 was one of the markedly upregulated long noncoding RNAs in the EHP group. Silencing of Mhrt779 attenuated the antihypertrophic effect of EHP in mice with TAC and in cultured cardiomyocytes treated with angiotensin II, and overexpression enhanced the antihypertrophic effect. By chromatin immunoprecipitation assay and qPCR, we found that EHP increased histone 3 trimethylation (H3K4me3 and H3K36me3) at a4 promoter of Mhrt779. Comprehensive identification of RNA-binding proteins by mass spectrometry and Western blot showed that Mhrt779 can bind Brg1 to upregulate Hdac2 and inhibit phosphorylation of Akt and GSK3β. Conclusions: Myocardial hypertrophy preconditioning evoked by exercise increases resistance to pathological stress via an antihypertrophic effect mediated by a signal pathway of Mhrt779 /Hdac2/p-Akt/p-GSK3β.
2020-11-07 | GSE161030 | GEO
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
Project description:The molecular mechanism underlying cardiac remodeling following myocardial infarction have been incompletely understood. Until now, most studies have been performed in rodents. We studied cardiac remodeling in the physiologically more relevant animal model, the swine. Microarray analysis was performed on animals that underwent either sham surgery or permanent ligation of the left coronary artery (MI). RNA was isolated from the remote, non-ischemic, regions of the left ventricle.
2011-12-21 | GSE27962 | GEO
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