Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA93809 | ENA |
REPOSITORIES: ENA
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Project description:Compensated and decompensated hypertrophy after monocrotaline injection
| PRJNA90675 | ENA
Project description:We recently introduced a modification of the established monocrotaline (MCT) model for pulmonary hypertension (PH) and subsequent right ventricular (RV) hypertrophy, which allows for the selective induction of either a compensate or decompensated RV hypertrophic phenotype within four weeks after a single subcutaneous MCT injection. Both doses of 30 or 80 mg/kg body weight lead to an intermediate phase of compensated RV hypertrophy (day 14-19), while the former dose leads to a stable compensated phenotype (HYP) and the latter dose progresses towards decompensated ventricular hypertrophy and RV failure (CHF) around day 25-28 (Buermans et. al, Physiological Genomics 2005). This model provides the unique opportunity to characterize the development of either hypertrophic phenotype during the very early stages after imposition of RV pressure overload remodeling, well before phenotypical differences have become apparent. This experiment series describes gene expression profiles, generated by spotted oligonucleotide microarrays, to characterize and compare the expression of ~4800 genes from the RV of HYP, CHF and time matched control rats at 10, 19 and 25 days after injections. RV samples were hybridized against a common reference pool, prepared from total RNA isolated from the interventricular septum wall from animals at day 19 and 25. Keywords: dose response x time course
2006-02-01 | GSE3675 | GEO
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:Cardiac hypertrophy is regulated by the zinc finger-containing DNA binding factors Gata4 and Gata6, both of which are required to mount a productive growth response of the adult heart. To determine if Gata4 and Gata6 are redundant or have non-overlapping roles, we performed cardiomyocyte-specific conditional gene deletions for Gata4 and Gata6 in conjunction with reciprocal replacement with a transgene encoding either Gata4 or Gata6, during the pressure overload response. We determined that Gata4 and Gata6 play a redundant and dosage-sensitive role in programming the hypertrophic growth response itself following pressure overload stimulation. However, non-redundant functions were identified as functional decompensation induced by either Gata4 or Gata6 deletion was not rescued by the reciprocal transgene, and only Gata4 heart-specific deletion produced a reduction in capillary density after pressure overload. Gene expression profiling from hearts of these gene-deleted mice showed both overlapping and unique transcriptional codes, with Gata4 exhibiting the strongest impact. These results indicate that Gata4 and Gata6 play a dosage-dependent and semi-redundant role in programming cardiac hypertrophy, but that each has a unique role in maintaining cardiac homeostasis and adaptation to injury that cannot be compensated by the other. Microarray-bassed gene expression profiling identified overlapping, distinct, and quantitatively/differentially regulated classes of Gata4 or Gata6 regulated genes. To determine if Gata4 and Gata6 are redundant or have non-overlapping roles in programming cardiac hypertrophic responses and adaptation to stress or injury, we performed cardiomyocyte-specific conditional gene deletions for Gata4 and Gata6 in conjunction with reciprocal replacement with a transgene encoding either Gata4 or Gata6, during the pressure overload response.
2014-01-01 | E-GEOD-52317 | biostudies-arrayexpress
Project description:Pressure overload (PO) leads first to cardiac hypertrophy and later to heart failure. In mice, PO leads to sex differences in cardiac morphology and function. However, early sex differences in gene regulation that precede sex differences in function have not yet been identified. To identify such changes, we developed a model of PO that is characterized by compensated hypertrophy without sex differences after 2 weeks and by heart failure with sex differences after 9 weeks. We used transverse aortic constriction (TAC) or sham-operation in male and female mice and analyzed gene expression by microarray experiments. Experiment Overall Design: The gene expression induced by pressure overload in female and male mice in comparison to sham operated control mice was investigated. For each of these four conditions four biological replicates were performed and the individual samples were hybridized seperately on Affymetrix RAE 430A GeneChip Arrays.
2008-06-15 | E-GEOD-6970 | biostudies-arrayexpress
Project description:Expression profiles at various time points after surgical intervention for pressure-overload induced cardiac hypertrophy and failure.
2004-06-30 | E-MEXP-105 | biostudies-arrayexpress
Project description:Background: BMPER, an orthologue of Drosophila melanogaster crossveinless-2, is a secreted factor that regulates BMP activity in endothelial cell precursors and during early cardiomyocyte differentiation. Although previously described in the heart, the role of Bmper in cardiac development and function remained unknown. Methods: BMPER deficient hearts were phenotyped histologically and functionally using echocardiography and Doppler analysis. Since BMPER -/- mice die perinatally, BMPER +/- mice were then challenged to pressure overload induced cardiac hypertrophy and hind limb ischemia to determine changes in angiogensis and regulation of cardiomyocyte size. Results: We identified for the first time the cardiac phenotype associated with BMPER haploinsufficiency. BMPER mRNA and protein are present in the heart during cardiac development through at least E14.5 but is lost by E18.5. BMPER +/- ventricles are thinner and less compact than sibling wild-type hearts. In the adult, BMPER +/- hearts present with decreased anterior and posterior wall thickness, decreased cardiomyocyte size, and an increase in cardiac vessel density. Despite these changes, BMPER +/- mice respond to pressure overload-induced cardiac hypertrophy challenge largely to the same extent as wild-type mice. Conclusion: BMPER appears to play a role in regulating both vessel density and cardiac development in vivo; however, BMPER haploinsufficiency does not result in marked effects on cardiac function or adaptation to pressure overload hypertrophy. Unpaired, two-condition experiment, wild-type vs BMPER+/- adult hearts. Biological replicates: 4 per condition.
2012-09-20 | E-GEOD-40983 | 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
2007-12-19 | E-GEOD-76 | biostudies-arrayexpress
Project description:Cardiac hypertrophy has been well-characterized at the level of transcription. During cardiac hypertrophy, genes normally expressed primarily during fetal heart development are re-expressed, and this fetal gene program is believed to be a critical component of the hypertrophic process. Recently, alternative splicing of mRNA transcripts has been shown to be temporally regulated during heart development, leading us to consider whether fetal patterns of splicing also reappear during hypertrophy.We hypothesized that patterns of alternative splicing occurring during heart development are recapitulated during cardiac hypertrophy. Here we present a whole-transcriptome study of isoform expression during pressure-overload cardiac hypertrophy induced by 10 days of transverse aortic constriction (TAC) in rats and in developing fetal rat hearts compared to sham-operated adult rat hearts, using high-throughput sequencing of poly(A) tail mRNA. Quantification of isoform expression in fetal rat hearts, pressure-overloaded rat hearts, and sham-operated rat hearts by Illumina GAIIx in triplicate
2013-05-14 | E-GEOD-42411 | biostudies-arrayexpress