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Developmental gene expression differences between neonatal and adult mouse atria and ventricles

ABSTRACT: We study the role of glycosylation in ion channel function. Specfically, we are focusing on how ion channel glycosylation modulates, controls, and impacts cardiac, skeletal muscle, and neuronal electrical activity. We wish to determine differences in gene expression through development and between the atria and ventricles of the mouse heart. Our data indicate differential sialylation directly affects voltage-gated sodium channel function through the developing heart in a chamber-specific manner. We wish to expand our findings to include other ion channels involved in the cardiac action potential, and to eventually create a map of the cardiac conduction system that details the role of differential glycosylation in cardiac excitability. Determining differential expression of the genes that regulate ion channel glycosylation is vital to these goals.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE27589 | GEO | 2011/03/02

SECONDARY ACCESSION(S): PRJNA138293

REPOSITORIES: GEO

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Developmental gene expression differences between neonatal and adult mouse atria and ventricles

Project description:We study the role of glycosylation in ion channel function. Specfically, we are focusing on how ion channel glycosylation modulates, controls, and impacts cardiac, skeletal muscle, and neuronal electrical activity. We wish to determine differences in gene expression through development and between the atria and ventricles of the mouse heart. Our data indicate differential sialylation directly affects voltage-gated sodium channel function through the developing heart in a chamber-specific manner. We wish to expand our findings to include other ion channels involved in the cardiac action potential, and to eventually create a map of the cardiac conduction system that details the role of differential glycosylation in cardiac excitability. Determining differential expression of the genes that regulate ion channel glycosylation is vital to these goals. We analyzed four sets of pooled RNA to be run in triplicate: one each from neonatal and adult mouse atria and ventricles.

2011-03-02 | E-GEOD-27589 | biostudies-arrayexpress

Expression data from normal atria and ventricles

2009-08-24 | GSE5266 | GEO

Transcription profiling of normal atria and ventricles

Project description:Pharmacological and gene ablation studies have demonstrated a crucial role of the cardiac natriuretic peptides (NP) hormones ANF and BNP in the maintenance of cardiovascular homeostasis. In addition, hypertension and chronic congestive heart failure are clinical entities that may be regarded as states of relative NP deficiency. Hence the study of the function of the endocrine heart is highly relevant. To identify genes that are related to the endocrine function of the heart we have conducted differential gene expression studies of the rat atria and ventricles using oligonucleotide arrays. Experiment Overall Design: The atrial appendages and the ventricular free walls were obtained from thirteen normal male Sprague Dawley rats. The total RNA was obtained from four pools of atrial and four pools of ventricular tissues. Four biological replicates for each muscle type were generated, i.e. 4 atrial replicates and 4 ventricular replicates.

2009-09-15 | E-GEOD-5266 | biostudies-arrayexpress

Identification of cardiac ion channel protein networks and their signature in the human electrocardiogram

Project description:Protein-protein interactions are essential for normal cellular processes and signaling events. Defining these interaction networks is therefore crucial for understanding complex cellular functions and interpretation of disease-associated gene variants. We need to build a comprehensive picture of the interactions, their affinities and interdependencies in the specific organ and cell-type to understand hitherto poorly understood signaling mechanism through ion channels and to begin their mechanistic studies. Here, we experimentally identify the ensemble of interacting partners for 13 types of ion channel in murine cardiac tissue to understand their role in cardiomyocyte electrophysiology. Of these, we validated the functional importance of 10 novel interactors on cardiac electrophysiology through genetic knockouts in zebrafish, super resolution microscopy, and patch clamp experiments. Furthermore, we establish a computational framework to reconstruct human cardiomyocyte ion channel networks from deep proteome mapping of human heart tissue and human heart single-cell gene-expression data. Finally, we integrate the ion channel interactome with human population genetics data to identify proteins that influence the electrocardiogram (ECG). The combined channel network is enriched for proteins influencing the ECG; with 44% of the network proteins significantly associated with an ECG phenotype. Altogether, we comprehensively define the interactomes of 13 major cardiac ion channels, contextualize their relevance to human electrophysiology including impact on the ECG, and validate the functional roles of ten novel interactors, thereby creating a roadmap for our understanding of how ion channel interactomes regulate cardiac electrophysiology.

2023-09-18 | PXD028021 | Pride

RNAseq of ST6GAL1-wild type and ST6GAL1-knock out cells of MDA-MB-231 cells.

Project description:Dynamic change of glycosylation is found in various cancers; however, the precise role of glycosylation in metastasis is remained largely unknown. Current study show that α2,6-sialylation or β-galactoside α2,6-sialyltransferase (ST6Gal1) inhibits circulating tumor cell aggregation and depletion or restoration of α2,6-sialylation in patient derived xenograft model amplified or diminished cell aggregation and lung metastasis.

2022-12-01 | GSE174080 | GEO

Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events [Figure 8 mRNA data]

Project description:Analysis of rhythmonome gene expression in cardiac myocytes derived from human induced pluripotent stem cells Cardiac electrical activity is controlled by the carefully orchestrated activity of more than a dozen different ion conductances. Yet, there is considerable variability in cardiac ion channel expression levels both within and between subjects. In this study we tested the hypothesis that variations in ion channel expression between individuals are not random but rather there are modules of co-expressed genes and that these modules make electrical signaling in the heart more robust. Meta-analysis of 3653 public RNA-Seq datasets identified a strong correlation between expression of CACNA1C (L-type calcium current, ICaL) and KCNH2 (rapid delayed rectifier K+ current, IKr), which was verified in mRNA extracted from human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CM). In silico modeling, validated with functional measurements in hiPSC-CM, indicates that the co-expression of CACNA1C and KCNH2 limits the variability in action potential duration and reduces susceptibility to early afterdepolarizations, a surrogate marker for pro-arrhythmia.

2020-03-10 | GSE146665 | GEO

Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events [Figure 2 mRNA data]

2020-03-10 | GSE146664 | GEO

MED13cTg heart ventricles and epididymal fat

Project description:The heart requires a continuous supply of energy but has little capacity for energy storage and thus relies on exogenous metabolic sources. We previously showed that cardiac MED13 modulates systemic energy homeostasis in mice. Here we sought to define the extra-cardiac tissue(s) that respond to cardiac MED13 signaling. We show that cardiac over-expression of MED13 in transgenic (MED13cTg) mice confers a lean phenotype that is associated with increased lipid uptake, beta-oxidation and mitochondrial content in white adipose tissue (WAT) and liver. Cardiac expression of MED13 decreases metabolic gene expression and metabolite levels in heart and liver but enhances them in WAT. Although exhibiting increased energy expenditure in the fed state, MED13cTg mice metabolically adapt to fasting. Furthermore, MED13cTg hearts oxidize fuel that is readily available, rendering them more efficient in the fed state. Parabiosis experiments in which circulations of wild-type and MED13cTg mice are joined, reveal that circulating factor(s) in MED13cTg mice promote enhanced metabolism and leanness. These findings demonstrate that MED13 acts within the heart to promote systemic energy expenditure in extra-cardiac energy depots and point to an unexplored metabolic communication system between the heart and other tissues.

2014-12-01 | GSE62450 | GEO

CYP2J2 Modulates Diverse Transcriptional Programs in Adult Human Cardiomyocytes

Project description:CYP2J2, a member of the Cytochrome P450 family of enzymes, is the most abundant epoxygenase in the heart and has multifunctional properties including bioactivation of epoxyeicosatrienoic acids, which, in turn, have been implicated in mediating several cardiovascular conditions. In order to elucidate the complex role played by CYP2J2 in cardiac tissue, we performed targeted silencing of CYP2J2 expression in human adult cardiomyoctes and interrogated whole genome transcriptional responses. We found that knockdown of CYP2J2 elicits widespread alterations in gene expression of ventricular cardiomyocytes and leads to the activation of a diverse repertoire of programs, including those involved in ion channel signaling, development, extracellular matrix, and metabolism. Several members of the differentially up-regulated ion channel module have well-known pathogenetic roles in cardiac dysrhythmias. By leveraging causal network and upstream regulator analysis, we identified several candidate drivers of the observed transcriptional response to CYP2J2 silencing; these master regulators have been implicated in aberrant cardiac remodeling, heart failure, and myocyte injury and repair. Collectively, our study demonstrates that CYP2J2 plays a central and multifaceted role in cardiomyocyte homeostasis, and provides a framework for identifying critical regulators and pathways influenced by this gene.

2020-03-07 | GSE136957 | GEO

Characterizing the global changes in miRNA expression in human atrial appendages with persistent atrial fibrillation.

Project description:Atrial fibrillation (AF), the most common cardiac rhythm disorder, is a major cause of cardiovascular morbidity and mortality. AF is characterized by the rapid and irregular activation of the atrium with diverse abnormalities, including electrical, structural, metabolic, neurohormonal, or molecular alterations.3 Although the pathophysiology of AF is complex, it has traditionally been treated with antiarrhythmic drugs that control the rhythm by altering cardiac electrical properties, principally by modulating ion channel function. However, treatments of AF with antiarrhythmic drugs have mostly failed to control the heart rhythm, because the electrical characteristics of atrial cardiomyocytes are eventually altered or remodeled during the course of AF. The aims of this study were to characterize the global changes in miRNA expression in human atrial appendages and to identify the target ion channel(s) responsible for electrical remodeling in AF. In this study, we performed a comprehensive analysis of miRNA microarrays, using a strict selection for human samples.

2017-04-25 | GSE68475 | GEO

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