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Differential gene expression between WT and ERRa-null hearts

ABSTRACT: Total RNA was isolated from 3 WT and 3 ERRa null hearts and independent hybridizations were performed using MOE430 2.0 microarrays. Expression profiling was conducted to determine changes in gene expression in hearts lacking ERRa. The expression of genes involved in heart and muscle development, muscle contraction, lipid metabolism, OxPhos, protein metabolism and transcription were affected by the loss of ERRa. Keywords: microarray and genetic modification

ORGANISM(S): Mus musculus

PROVIDER: GSE7196 | GEO | 2007/03/08

SECONDARY ACCESSION(S): PRJNA98241

REPOSITORIES: GEO

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Transcription profiling of mouse hearts from mutants lacking estrogen-related receptor alpha (ERRalpha), a nuclear receptor

Project description:Total RNA was isolated from 3 WT and 3 ERRalpha null hearts and independent hybridizations were performed using MOE430 2.0 microarrays. Expression profiling was conducted to determine changes in gene expression in hearts lacking ERRa. The expression of genes involved in heart and muscle development, muscle contraction, lipid metabolism, OxPhos, protein metabolism and transcription were affected by the loss of ERRa. Experiment Overall Design: 3 hearts from WT and 3 hearts from ERRalpha-null mice were used in the study. The expression of genes in the ERRalpha KO hearts were compared to the reference WT hearts.

2007-11-10 | E-GEOD-7196 | biostudies-arrayexpress

ERRa/ERRg KO heart gene expression analysis

Project description:ERRa and ERRg are essential transcriptional regulators of cardiac metabolism and functions. Here we extend our previous studies by analyzing the transcriptome changes in ERRa/ERRg KO hearts

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RNA-Seq transcriptome profiling of postnatal age 35 days or P35 ventricles of cardiac-specific estrogen-related receptor alpha and gamma (ERRa/g) knock down (KD) mouse generated by AAV-cTnT-Cre injection and its control AAV-Luc injection.

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RNA-Seq transcriptome profiling of embryonic age 17.5 or E17.5 ventricles of cardiac specific-estrogen-related receptor alpha and gamma (ERRa/g) knock out (KO) mouse generated by Nkx2.5-Cre driver and its control wild type.

Project description:Transcriptional regulatory circuits that drive cardiomyocyte maturation during the developmental process are poorly understood. Estrogen-related receptor alpha and gamma (ERRa/g) have been shown to be involved in all aspects of mitochondrial energy production. However, the function of ERR during the cardiac developmental process is not understood well. To examine the role of (ERRa/g), we generated cardiac-specific ERRa/g knockout (KO) mice and found that the KO mice died within 24 hours post-birth. At embryonic age 17.5, a number of genes involved in oxidative mitochondrial metabolism including OXPHOS, TCA cycle, and fatty acid oxidation were dramatically downregulated. Also, the mutant hearts exhibited a significant downregulation of adult cardiac contractile protein, ion channel and Ca2+ handling genes. In contrast, fetal cardiac genes and non-cardiac genes that express in fibroblast or endothelial cells were ectopically induced in the KO hearts. These results suggest that ERRa/g are essential factors for the broad cardiomyocyte maturation program.

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ERRalpha wt vs. ko hearts, baseline

Project description:We hypothesized that the estrogen-related receptor a (ERRa), which recruits PGC-1a to metabolic target genes in heart, exerts protective effects in the context of stressors known to cause heart failure. ERRa-/- mice subjected to left ventricular (LV) pressure overload developed signatures of heart failure including chamber dilatation and reduced LV fractional shortening. 31P-NMR studies revealed abnormal phosphocreatine depletion in ERRa-/- hearts subjected to hemodynamic stress, indicative of a defect in ATP reserve. Mitochondrial respiration studies demonstrated reduced maximal ATP synthesis rates in ERRa-/- hearts. Cardiac ERRa target genes involved in energy substrate oxidation, ATP synthesis, and phosphate transfer were downregulated in ERRa-/- mice at baseline or with pressure overload. These results demonstrate that ERRa, a potential therapeutic target, is indispensable for the adaptive bioenergetic response to hemodynamic stressors known to cause heart failure. Keywords: Genetic modification, stress response

2007-10-16 | GSE8106 | GEO

Transcription profiling of mouse ERRalpha wild type vs. knockout hearts, baseline

2008-06-15 | E-GEOD-8106 | biostudies-arrayexpress

Role of estrogen related receptor alpha (ERRa) in CD4+ T cell gene expression

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2011-10-20 | E-GEOD-33108 | biostudies-arrayexpress

Endoplasmic Reticulum Stress-mediated Mitochondrial Dysfunction in Aged Hearts

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M1BP RNAi during Drosophila flight myogenesis: Analyses at 2-day adult stage

Project description:Oxidative metabolism is the predominant energy source for muscle contraction. How this is transcriptionally regulated during muscle development to accommodate different metabolic requirements and muscle types is largely unknown. We show that the formation of mitochondria cristae harbouring the respiratory chain is concomitant with a large-scale transcriptional upregulation of genes linked with oxidative phosphorylation (OXPHOS) during the middle of Drosophila flight muscle development. We further demonstrate using high-resolution imaging, transcriptomic and biochemical analyses that Motif-1-binding protein (M1BP) transcriptionally regulates the expression of genes encoding critical components for OXPHOS complex assembly and integrity. In the absence of M1BP, mitochondrial respiratory complexes are improperly assembled and aggregate in the mitochondrial matrix, triggering a strong protein quality control response. Together, this study provides the first insight into the transcriptional regulation of oxidative metabolism during Drosophila myogenesis and identifies M1BP as a novel player in this process.

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