WT and Hira-null undifferentiated mESCs and day15 differentiated cardiomyocytes
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ABSTRACT:
PROVIDER: PRJNA438521 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: The goals of this study are to compare transcriptome profiling (RNA-seq) resulting from the knockout of Hira in undifferentiated mouse embryonic stem cells (mESCs) and in day 15 differentiated cardiomyocytes.Methods: RNA extraction was done in duplicate from WT and Hira-null mESCs at day0 and day15 using TRIzol reagent. RNAseq was done onIllumina Nextseq500 and processed by the ICH genomics facility, reads were aligned and normalised using BOWTIE and DEseq R2 package. Gene lists were filtered using adjusted p-value ≤ 0.05 and absolute fold change ≥ 2. Results:We identified 1680 transcripts changed in the absence of HIRA in day 15 differentiated cardiomyocytes. GO term cardiovascular system development was the most downregulated gene set(p-value ≤ 0.01 and FDR ≤0.1. Conclusion: this study analysis the role of HIRA in early cardiac mesoderm development usinf an invitro mESCs model.
2019-04-01 | GSE111910 | GEO
Project description:HIRA is a histone chaperone that modulates gene expression through the deposition of H3.3. Conditional knockout of Hira in embryonic mouse hearts leads to cardiac septal defects. However, the effects of HIRA on the gene expression profile at earlier stages of cardiogenic mesoderm differentiation has not yet been studied. Differentiation of mouse embryonic stem cells (mESCs) towards cardiomyocytes mimics some of these events and is an accepted model of these early stages. We performed RNA-Seq and H3.3-HA ChIP-seq on both WT and Hira-null mESCs and early cardiomyocyte progenitors of both genotypes. Analysis of our RNA-seq data showed differential down regulation of cardiovascular development-related genes in Hira-null cardiomyocytes compared to WT cardiomyocytes. Correlating these data with H3.3 enrichment showed that HIRA is required for the expression of the transcription factors (TFs) Gata6, Meis1 and Tbx2. These TFs displayed diminished HIRA-dependent H3.3 enrichment in their gene bodies or at their transcription start site in the absence of HIRA. Our results reveal new transcription factors through which HIRA influences cardiogenesis in vitro and potentially in vivo.
2019-01-18 | GSE112078 | GEO
Project description:Hira has been implicated in replication-independent chromatin assembly. To determine the role of Hira in the regulation of embryonic stem (ES) cell gene expression, we used microarrays to analyze the global program of gene expression in Hira null versus WT undifferentiated ES cells.
2009-12-19 | GSE19542 | GEO
Project description:Genome-wide gene expression analysis at different stages of cardiomyocyte differentiation (undifferentiated mouse embryonic stem cells, neonatal mouse cardiomyocytes and adult mouse cardiomyocytes). Results provide important information on the differential expressed genes between undifferentiated mouse embrionic stem cells (mES) and mouse cardiomyocytes (CM) and also between cardiomyocytes from neonatal (CMp) and adult stages (CMa). This dataset allowed us to compare the expression profile of mES, CMp and CMa with the epigenetic profile of histone methylation generated with ChIP-seq experiments. Total RNA was obtained from biological triplicate of undifferentiated mouse embryonic stem cells (mES), neonatal mouse cardiomyocytes (CMp) and adult mouse cardiomyocytes (CMa)
2014-12-22 | E-GEOD-44829 | biostudies-arrayexpress
Project description:Genome-wide gene expression analysis at different stages of cardiomyocyte differentiation (undifferentiated mouse embryonic stem cells, neonatal mouse cardiomyocytes and adult mouse cardiomyocytes). Results provide important information on the differential expressed genes between undifferentiated mouse embrionic stem cells (mES) and mouse cardiomyocytes (CM) and also between cardiomyocytes from neonatal (CMp) and adult stages (CMa). This dataset allowed us to compare the expression profile of mES, CMp and CMa with the epigenetic profile of histone methylation generated with ChIP-seq experiments.
2014-12-22 | GSE44829 | GEO
Project description:We performed gene expression profiling by microarray using RNA extracted from healthy free wall left ventricle tissues from control and Hira cardiomyocyte-specific conditional knockout mice at 6 weeks of age. Hira is a histone chaperone responsible for replication-independent incorporation of histone variant H3.3 at actively transcribed regions. Conditional knockout of Hira in cardiomyocytes resulted in impaired cardiac function, cardiomyocyte degeneration and focal replacement fibrosis. These results illustrate the role of Hira in controlling the cardiac gene program. 4 animals per group (control and Hira conditional knockout) hybridized in triplicate. RNA was extracted from healthy free wall left ventricle.
2016-04-06 | E-GEOD-71833 | biostudies-arrayexpress
Project description:We performed gene expression profiling by microarray using RNA extracted from healthy free wall left ventricle tissues from control and Hira cardiomyocyte-specific conditional knockout mice at 6 weeks of age. Hira is a histone chaperone responsible for replication-independent incorporation of histone variant H3.3 at actively transcribed regions. Conditional knockout of Hira in cardiomyocytes resulted in impaired cardiac function, cardiomyocyte degeneration and focal replacement fibrosis. These results illustrate the role of Hira in controlling the cardiac gene program.
2016-04-06 | GSE71833 | GEO
Project description:We subjected podocytes (either differentiated or undifferentiated) to a pulse with stable isotope labeled amino acids for 24, 48, 72 and 96h.
2018-05-01 | PXD006887 | Pride
Project description:Media conditioned by undifferentiated human embryonic stem cells enhanced karyokinesis, cytokinesis and cell proliferation in cultures of differentiated, beating primary rat cardiomyocytes without altering their final contractile phenotype. Transcriptome analysis of proliferating cardiomyocytes revealed comprehensive activation of the ROCK 1 and 2 G-protein coupled receptor (GPCR) pathway associated with cytokinesis, and the RAS/RAF/MEK/ERK receptor tyrosine kinase pathways (RTK) and JAK/STAT-cytokine pathway involved in cell cycle progression. Correlative multi-analyte profiling (85 proteins) of conditioned media identified 33 proteins at significantly elevated levels compared to unconditioned media including ligands specific to the GPCR signal transduction pathways (serum amyloid A, monocyte chemoattractant protein-1, macrophage inhibitory protein, IL-8, macrophage inflammatory protein 1-alpha, eotaxin), RTK activation (IGFbp-1, IGFbp-2, HGF) and JAK-STAT stimulation pathways (IL-6, IFNa) activated in the treated cardiomyocytes. These data indicated that ES cells secreted a unique admixture of factors associated with induction of mitotic replication, cytokinesis and proliferation in cardiomyocytes.
2010-06-01 | GSE13708 | GEO
Project description:The self-renewing pluripotent state was first captured in mouse embryonic stem cells (mESCs) over two decades ago. The standard condition requires the presence of serum and LIF, which provide growth promoting signals for cell expansion. However, there are pro-differentiation signals which destabilize the undifferentiated state of mESCs. The dual inhibition (2i) of the pro-differentiation Mek/Erk and Gsk3/Tcf3 pathways in mESCs is sufficient to establish an enhanced pluripotent “ground state” which bears features resembling the pre-implantation mouse epiblast. Gsk3 inhibition alleviates the repression of Esrrb, a transcription factor that can substitute for Nanog function in mESCs. The molecular mechanism that is mediated by Mek inhibition is however not clear. In this study, we investigate the pathway through which Mek inhibition operates to maintain ground state pluripotency. We have found that in mESCs, Kruppel-like factor 2 (Klf2) is a protein target of the Mek/Erk pathway; and that Klf2 protein is phosphorylated by Erk2 and subsequently degraded through the proteosome. It is therefore by Mek-inhibition through PD0325901 or 2i that enables the stabilization and accumulation of Klf2 to sustain ground state pluripotency. Importantly, we found that Klf2-null mESCs, while viable under LIF/Serum conditions, cannot be maintained and eventually gradually die within a few passages. Our result thus demonstrates that Klf2 is an essential factor of ground state pluripotency. Collectively, our study defines the Mek/Klf2 axis that cooperates with the Gsk3/Esrrb pathway in mediating ground state pluripotency.
2014-06-04 | E-MTAB-2366 | biostudies-arrayexpress