Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA227330 | ENA |
REPOSITORIES: ENA
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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: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:Cardiac left ventricular physiological hypertrophy in swine
| PRJNA165671 | ENA
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
2007-12-19 | E-GEOD-76 | biostudies-arrayexpress
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
Project description:NHLBI TOPMed: HyperGEN: Genetics of Left Ventricular Hypertrophy
| PRJNA371676 | ENA
Project description:NHLBI TOPMed: HyperGEN: Genetics of Left Ventricular Hypertrophy
| PRJNA371675 | ENA
Project description:The right ventricle (RV) differs in several aspects from the left ventricle (LV) including its embryonic origin, physiological role and anatomical design. In contrast to LV hypertrophy, little is known about the molecular circuits, which are activated upon RV hypertrophy (RVH). We established a highly reproducible model of RVH in mice using pulmonary artery clipping (PAC), which avoids detrimental RV pressure overload and thus allows long-term survival of operated mice. Magnetic resonance imaging revealed pathognomonic changes with striking similarities to human congenital heart disease- or pulmonary arterial hypertension- patients. Comparative, microarray based transcriptome analysis of right- and left-ventricular remodeling identified distinct transcriptional responses to pressure-induced hypertrophy of either ventricle, which were mainly characterized by stronger transcriptional responses of the RV compared to the LV myocardium. Hierarchic cluster analysis revealed a RV- and LV-specific pattern of gene activity after induction of hypertrophy, however, we did not find evidence for qualitatively distinct regulatory pathways in RV compared to LV. Data mining of nearly three thousand RV-enriched genes under PAC disclosed novel potential (co)-regulators of long-term RV remodeling and hypertrophy. We reason that specific inhibitory mechanisms in RV restrict excessive myocardial hypertrophy and thereby contribute to its vulnerability to pressure overload.
2011-07-07 | GSE30428 | GEO
Project description:The right ventricle (RV) differs in several aspects from the left ventricle (LV) including its embryonic origin, physiological role and anatomical design. In contrast to LV hypertrophy, little is known about the molecular circuits, which are activated upon RV hypertrophy (RVH). We established a highly reproducible model of RVH in mice using pulmonary artery clipping (PAC), which avoids detrimental RV pressure overload and thus allows long-term survival of operated mice. Magnetic resonance imaging revealed pathognomonic changes with striking similarities to human congenital heart disease- or pulmonary arterial hypertension- patients. Comparative, microarray based transcriptome analysis of right- and left-ventricular remodeling identified distinct transcriptional responses to pressure-induced hypertrophy of either ventricle, which were mainly characterized by stronger transcriptional responses of the RV compared to the LV myocardium. Hierarchic cluster analysis revealed a RV- and LV-specific pattern of gene activity after induction of hypertrophy, however, we did not find evidence for qualitatively distinct regulatory pathways in RV compared to LV. Data mining of nearly three thousand RV-enriched genes under PAC disclosed novel potential (co)-regulators of long-term RV remodeling and hypertrophy. We reason that specific inhibitory mechanisms in RV restrict excessive myocardial hypertrophy and thereby contribute to its vulnerability to pressure overload. Alternative splicing and gene expression analysis during development of the heart and cardiomyoyte differentiation.
2011-07-07 | E-GEOD-30428 | biostudies-arrayexpress
Project description:To identify novel targets in left ventricular (LV) hypertrophy (LVH) we initiated comparative transcriptome analysis between genetic models derived from stroke-prone spontaneously hypertensive rats (SHRSP) and Fischer (F344). Previous genetic studies in the SHRSP/F344 model confirmed the presence of a major quantitative trait locus (QTL) for LV mass on rat chromosome (RNO) 1. We assigned carboxypeptidase X 2 (Cpxm2) to a genetic locus for LV mass identified in SHRSP. We assigned carboxypeptidase X 2 (Cpxm2) to a genetic locus for left ventricular mass.
2023-07-10 | GSE154326 | GEO