Chromatin landscape in perinatal cardiomyocytes
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ABSTRACT:
ORGANISM(S): Mus musculus Rattus norvegicus
PROVIDER: GSE178673 | GEO | 2023/02/03
REPOSITORIES: GEO
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Project description:Chromatin landscape in perinatal cardiomyocytes
| PRJNA739989 | ENA
Project description:To date, there have been limited high quality libraries of cardiomyocyte maturation during the perinatal period, in part owing to the difficulty of isolating large perinatal cardiomyocytes. We previously developed a method utilizing large-particle fluorescent activated cell sorting (LP-FACS) to isolate adult cardiomyocytes for single cell RNA-seq (Kannan et al., Circ Res, 2019). We utilize this method to generate a reference of perinatal cardiomyocyte maturation.
2020-04-01 | GSE147807 | GEO
Project description:β-Catenin signaling pathway regulates cardiomyocytes proliferation and differentiation, though its involvement in metabolic regulation of cardiomyocytes remains unknown. We used one-day-old mice with cardiac-specific knockout of β-catenin and neonatal rat ventricular myocytes treated with β-catenin inhibitor to investigate the role of β-catenin metabolism regulation in perinatal cardiomyocytes. Transcriptomics of perinatal β-catenin-ablated hearts revealed a dramatic shift in the expression of genes involved in metabolic processes. Further analysis indicated an inhibition of lipolysis and glycolysis in both in vitro and in vivo models. Finally, we showed that β-catenin deficiency leads to mitochondria dysfunction via the downregulation of Sirt1/PGC-1α pathway. We conclude that cardiac-specific β-catenin ablation disrupts the energy substrate shift that is essential for postnatal heart maturation, leading to perinatal lethality of homozygous β-catenin knockout mice.
2021-08-31 | GSE153995 | GEO
Project description:In this study, we generated nucleotide-resolution translatome as well as transcriptome data of isolated primary cardiomyocytes undergoing hypertrophy. More than 10,000 open reading frames (ORF) were detected from the deep sequencing of ribosome protected fragments orchestrating the shift of translatome in hypertrophied cardiomyocytes.We further identified more than 100 potential micropeptides encoded by uncharacterized small open reading frames (sORFs) in the long noncoding RNA genes. Over two-thirds of these micropeptide candidates were experimentally validated in a random test with three micropeptides showing regulatory function in cardiomyocyte hypertrophy via modulating the activities of Oxidative phosphorylation, Calcium signaling pathway, and MAPK signaling pathway.Our study provided a genome-wide overview of the translational controls of cardiomyocyte hypertrophy and demonstrated an unrecognized role of micropeptides in cardiomyocyte biology.
2021-03-11 | GSE155912 | GEO
Project description:In this study, we generated nucleotide-resolution translatome as well as transcriptome data of isolated primary cardiomyocytes undergoing hypertrophy. More than 10,000 open reading frames (ORF) were detected from the deep sequencing of ribosome protected fragments orchestrating the shift of translatome in hypertrophied cardiomyocytes.We further identified more than 100 potential micropeptides encoded by uncharacterized small open reading frames (sORFs) in the long noncoding RNA genes. Over two-thirds of these micropeptide candidates were experimentally validated in a random test with three micropeptides showing regulatory function in cardiomyocyte hypertrophy via modulating the activities of Oxidative phosphorylation, Calcium signaling pathway, and MAPK signaling pathway.Our study provided a genome-wide overview of the translational controls of cardiomyocyte hypertrophy and demonstrated an unrecognized role of micropeptides in cardiomyocyte biology.
2021-03-11 | GSE155913 | GEO
Project description:In this study, we generated nucleotide-resolution translatome as well as transcriptome data of isolated primary cardiomyocytes undergoing hypertrophy. More than 10,000 open reading frames (ORF) were detected from the deep sequencing of ribosome protected fragments orchestrating the shift of translatome in hypertrophied cardiomyocytes.We further identified more than 100 potential micropeptides encoded by uncharacterized small open reading frames (sORFs) in the long noncoding RNA genes. Over two-thirds of these micropeptide candidates were experimentally validated in a random test with three micropeptides showing regulatory function in cardiomyocyte hypertrophy via modulating the activities of Oxidative phosphorylation, Calcium signaling pathway, and MAPK signaling pathway.Our study provided a genome-wide overview of the translational controls of cardiomyocyte hypertrophy and demonstrated an unrecognized role of micropeptides in cardiomyocyte biology.
2021-03-11 | GSE155899 | GEO
Project description:The direct conversion, or trans-differentiation, of non-cardiac cells into cardiomyocytes by forced expression of transcription factors and microRNAs provide promising ways of cardiac regeneration. However, genetic manipulations are still not desirable in real clinical applications. we report the generation of automatically beating cardiomyocyte-like cells from mouse fibroblasts with only chemical cocktails. These chemical-induced cardiomyocyte-like cells (CiCMs) express cardiomyocyte-specific markers, exhibit sarcomeric organization, and possess typical cardiac calcium flux and electrophysiological features. Microarray-bassed gene expression patterns of Mouse embryonic fibroblasts (MEFs), CiCMs, and cardiomyocytes(CMs) indicated a clear transition from dividing MEFs to differentiated cardiomyocyte-like state in CiCM samples. Mouse embryonic fibroblasts were treated with a small-molecule combination CRFVPT (10 μM CHIR99021 (C); 10 μM RepSox (R); 50 μM Forskolin (F); 0.5 mM VPA (V); 5 μM Parnate, (P); 1 μM TTNPB (T)) to induce transdifferentiation to chemical-induced cardiomyocyte-like cells. CiCMs beating clusters were picked at day 24 for analysis. MEFs were isolated from mouse embryos, and CMs were isolated from mouse hearts. Total RNA of MEFs, CiCMs and CMs were extracted and hybridization on Affymetrix microarrays.
2015-08-23 | E-GEOD-69924 | biostudies-arrayexpress
Project description:Heart disease remains the leading cause of death globally. Although reperfusion following myocardial ischemia can prevent death by restoring nutrient flow, ischemia/reperfusion injury can cause significant heart damage. The mechanisms that drive ischemia/reperfusion injury are not well understood; currently, few methods can predict the state of the cardiac muscle cell and its metabolic conditions during ischemia. Here, we explored the energetic sustainability of cardiomyocytes, using a model for cellular metabolism to predict the levels of ATP following hypoxia. We modeled glycolytic metabolism with a system of coupled ordinary differential equations describing the individual metabolic reactions within the cardiomyocyte over time. Reduced oxygen levels and ATP consumption rates were simulated to characterize metabolite responses to ischemia. By tracking biochemical species within the cell, our model enables prediction of the cell’s condition up to the moment of reperfusion. The simulations revealed a distinct transition between energetically sustainable and unsustainable ATP concentrations for various energetic demands. Our model illustrates how even low oxygen concentrations allow the cell to perform essential functions. We found that the oxygen level required for a sustainable level of ATP increases roughly linearly with the ATP consumption rate. An extracellular O2 concentration of ~0.007 mM could supply basic energy needs in non-beating cardiomyocytes, suggesting that increased collateral circulation may provide an important source of oxygen to sustain the cardiomyocyte during extended ischemia. Our model provides a time-dependent framework for studying various intervention strategies to change the outcome of reperfusion.
2024-09-02 | BIOMD0000000961 | BioModels
Project description:The direct conversion, or trans-differentiation, of non-cardiac cells into cardiomyocytes by forced expression of transcription factors and microRNAs provide promising ways of cardiac regeneration. However, genetic manipulations are still not desirable in real clinical applications. we report the generation of automatically beating cardiomyocyte-like cells from mouse fibroblasts with only chemical cocktails. These chemical-induced cardiomyocyte-like cells (CiCMs) express cardiomyocyte-specific markers, exhibit sarcomeric organization, and possess typical cardiac calcium flux and electrophysiological features. Microarray-bassed gene expression patterns of Mouse embryonic fibroblasts (MEFs), CiCMs, and cardiomyocytes(CMs) indicated a clear transition from dividing MEFs to differentiated cardiomyocyte-like state in CiCM samples.
2015-08-23 | GSE69924 | GEO
Project description:Exclusion of Parkin from mitochondria of perinatal cardiomyocytes interrupts structural and molecular transformations essential to normal perinatal-adult mitochondrial replacement. mRNA-sequencing from cardiac total RNA was performed at P1, P21 and 5-week stages of nontransgenic (ntg) and human-Mfn2-overexpressing (Mfn2wt) hearts, and also of tet-off control (tetoff) and human-Mfn2 T111A/S442A-overexpressing (Mfn2AA) hearts.
2015-12-04 | GSE68921 | GEO