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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

2017-05-05 | GSE88761 | GEO

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.

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 postnatal cardiac developmental process is unclear. To examine the role of (ERRa/g) during postnatal cardiac maturation, we generated inducible cardiac-specific ERRa/g knockdown (KD) mice with adeno-associated virus serotype 9 (AAV9) expressing Cre. We found that at P35 a number of genes involved in oxidative mitochondrial metabolism including OXPHOS, TCA cycle, branched chain amino acid catabolism, and fatty acid oxidation were dramatically downregulated. Also, the KD 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 skeletal muscle cells were ectopically induced in the KD hearts. These results suggest that ERRa/g are essential factors for the broad postnatal cardiomyocyte maturation program.

2020-06-10 | GSE135347 | GEO

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.

2020-06-10 | GSE113761 | GEO

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

2011-10-21 | GSE33108 | GEO

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

Project description:ERRa is an orphan nuclear receptor with an established role in cell metabolism. Our studies demonstrate that acute or chronic loss of ERRa broadly affects mitochondrial and glycolytic metabolism in CD4+ T cells and results in diminished T cell function and differentation. In this array, we assessed the contribution of ERRa to changes in gene expression in resting and stimulated CD4+ T cells with the goal of identifying specific metabolic genes that exhibit altered expression in the presence or absence of ERRa. Please see related publication: Michalek, et al. PNAS 2011. CD4+ T cells from 6-8 week old mice were negatively selected (Miltenyi), resulting in >95% purity and cultured in RPMI 1640 (Mediatech) with 10% FBS (Gemini Bio-Products). Wild-type (WT) and ERRa−/− (ERRKO) CD4+ T cells were harvested directly ex vivo or stimulated with anti-CD3 and anti-CD28 antibodies for 12 h in the presence or absence of the pharmacological inhibtors of ERRa XCT790 and Compound A. RNA was harvested using the RNeasy Plus kit from Qiagen.The microarray was prepared and analyzed by the Duke Microarray Facility using Ambion Message Amp Premier labeling and Affymetrix GeneChip Mouse Genome 430A 2.0. Each assay contains three independent biologic replicates.

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

Endoplasmic Reticulum Stress-mediated Mitochondrial Dysfunction in Aged Hearts

Project description:Aging impairs the mitochondrial electron transport chain (ETC), especially in interfibrillar mitochondria (IFM). Mitochondria are in close contact with the endoplasmic reticulum (ER). Induction of ER stress leads to ETC injury in adult heart mitochondria. We asked if ER stress contributes to the mitochondrial dysfunction during aging. Subsarcolemmal mitochondria (SSM) and IFM were isolated from 3, 18, and 24 mo. C57Bl/6 mouse hearts. ER stress progressively increased with age, especially in 24 mo. mice that manifest mitochondrial dysfunction. OXPHOS was decreased in 24 mo. IFM oxidizing complex I and complex IV substrates. Proteomic analysis showed that the content of multiple complex I subunits was decreased in IFM from 24 mo. hearts, but remained unchanged in in 18 mo. IFM without a decrease in OXPHOS. Feeding mice with 4-phenylbutyrate (4-PBA) for two weeks attenuated the ER stress and improved mitochondrial function in 24 mo. mice. These results indicate that ER stress contributes to the mitochondrial dysfunction in aged hearts. Attenuation of ER stress is a potential approach to improve mitochondrial function in aged hearts.

2020-07-23 | PXD018545 | Pride

Assay for transposase-accessible chromatin sequencing (ATAC-seq) on estrogen-related receptor alpha and gamma (ERRa/g) knock out (KO) human iPS cell-derived cardiomyocytes (hiPSC-CMs)

Project description:To determine the role of estrogen-related receptor alpha and gamma (ERRa/g) on chromatin accessibility, we performed ATAC-seq studies with WT control and ERRa/g KO hiPSC-CMs. We found that ERRa/g activates cardiac chromatin accessibilities in hiPSC-CMs. A subset of the decreased ATAC signals by loss of ERRa/g overlapped ERRg peaks (GSE113760) in hiPSC-CMs, suggesting that ERRg might be directly involved in the activation of cardiac chromatin accessibilities. The motif analysis with decreased ATAC signal by loss of ERRa/g revealed that cardiac-enriched transcription factors such as MEF2 and GATA could cooperate with ERR.

2022-02-16 | GSE165962 | GEO

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