Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA113231 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Findings suggest that PPARalpha plays a decisive role in the development of hypertrophy, affecting the functional outcome of the heart. Unfortunately, information on the nature of PPARalpha-dependent processes in cardiac hypertrophy is fragmentary and incomplete. The primary aim of this study was to identify the processes and signaling pathways regulated by PPARalpha in hearts challenged by a chronic pressure overload by means of whole genome transcriptomic analysis. Second, we wanted to gain insight how PPARalpha modulates the identified processes, e.g. by trans-activation or by trans-repression. Keywords: 28 days of TAC
2008-08-06 | GSE12337 | GEO
Project description:Findings suggest that PPARalpha plays a decisive role in the development of hypertrophy, affecting the functional outcome of the heart. Unfortunately, information on the nature of PPARalpha-dependent processes in cardiac hypertrophy is fragmentary and incomplete. The primary aim of this study was to identify the processes and signaling pathways regulated by PPARalpha in hearts challenged by a chronic pressure overload by means of whole genome transcriptomic analysis. Second, we wanted to gain insight how PPARalpha modulates the identified processes, e.g. by trans-activation or by trans-repression. Experiment Overall Design: Wild-type and PPARalpha-/- mice were sham-operated or subjected to TAC for 28 days. Left ventricular gene expression profile was determined using Affymetrix 430 2.0 arrays containing over 45,000 probe sets (covering over 34,000 mouse genes) to detect PPARalpha-related differences in cardiac gene expression under basal conditions and after imposition of a sustained hemodynamic stress.
2008-10-21 | E-GEOD-12337 | biostudies-arrayexpress
Project description:Cardiac-specific PPARalpha transgenic (Tg-PPARalpha) mice show mild cardiac hypertrophy and systolic dysfunction. The failing heart phenotypes observed in Tg-PPARalpha are exacerbated by crossing with cardiac-specific Sirt1 transgenic (Tg-Sirt1) mice, whereas Tg-Sirt1 mice themselves do not show any cardiac hypertrophy or systolic dysfunction. To investigate the mechanism leading to the failing heart phenotypes in TgPPARalpha/Tg-Sirt1 bigenic mice, microarray analyses were performed. The microarray analyses revealed that many ERR target genes were downregulated in Tg-PPARalpha and in Tg-Sirt1, and they were further downregulated in the Tg-PPARalpha/Tg-Sirt1 bigenic mice.
2011-12-01 | GSE33101 | GEO
Project description:Cardiac-specific PPARalpha transgenic (Tg-PPARalpha) mice show mild cardiac hypertrophy and systolic dysfunction. The failing heart phenotypes observed in Tg-PPARalpha are exacerbated by crossing with cardiac-specific Sirt1 transgenic (Tg-Sirt1) mice, whereas Tg-Sirt1 mice themselves do not show any cardiac hypertrophy or systolic dysfunction. To investigate the mechanism leading to the failing heart phenotypes in TgPPARalpha/Tg-Sirt1 bigenic mice, microarray analyses were performed. The microarray analyses revealed that many ERR target genes were downregulated in Tg-PPARalpha and in Tg-Sirt1, and they were further downregulated in the Tg-PPARalpha/Tg-Sirt1 bigenic mice. Four groups of cardiac-specific transgenic mice were used for the study, i.e., control, PPARalpha, Sirt1 and PPARalpha/Sirt1. Hearts were dissected after 10-11 weeks of male FVB background transgenic mice. Total RNA was prepared from the hearts to conduct the microarray analyses.
2011-12-01 | E-GEOD-33101 | biostudies-arrayexpress
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