Expression data from human embryonic stem cells(hESCs)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE38662 | GEO | 2014/06/30
SECONDARY ACCESSION(S): PRJNA168456
REPOSITORIES: GEO
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Project description:To detect the effect of early culture on hESCs, almost all initial-passaged hESCs have normal expression of DLK1-DIO3 gene cluster, the low-passaged hESCs lost the expression of DLK1-DIO3 gene cluster. hESCs were extracted for RNA with TriZOL and hybridization on Affymetrix arrays
2014-06-30 | E-GEOD-38662 | biostudies-arrayexpress
Project description:Pluripotent stem cells are increasingly used for therapeutic models, including transplantation of neural progenitors derived from human embryonic stem cells (hESCs). Recently, long non-coding RNAs (lncRNAs), including Maternally Expressed Gene 3 (MEG3) that is derived from DLK1-DIO3 imprinted locus, were found to be expressed during neural developmental events. Their deregulations are associated with various neurological diseases. The DLK1-DIO3 imprinted locus encodes abundant non-coding RNAs (ncRNAs) that are regulated by differential methylation on the locus. The aim of our research is to study the correlation between the DLK1-DIO3 derived ncRNAs and the capacity of hESC neural lineage differentiation. We classified hESCs into MEG3-ON and MEG3-OFF based on the expression levels of MEG3 as well as its downstream miRNAs by qRT-PCR. Initial embryoid body (EB) formation was conducted to examine the three germ layer differentiation ability. cDNA microarray was used to analyze the gene expression profiles of hESCs. Directed neural lineage differentiation was performed, followed by analysis of neural lineage marker expression levels and neurite formation via qRT-PCR and immunocytochemistry methods to investigate the capacity of neural differentiation in MEG3-ON and MEG3-OFF hESCs To study the correlations between the DLK1-DIO3 derived ncRNAs and differentiation capacity of hESC toward neural lineage, we classified hESCs into MEG3-ON and MEG3-OFF based on the expression levels of MEG3 by qRT-PCR and validated the methylation patterns of DLK1-DIO3 locus by bisulfite-sequencing. Then we conducted transcriptome analysis of these two groups of hESCs by cDNA microarray. This set contained 12 microarray samples, including 4 MEG3-ON hESCs, 7 MEG3-OFF hESCs, and 1 embryoid body as the negative control of pluripotentcy for pluritest.
2014-11-05 | E-GEOD-58809 | biostudies-arrayexpress
Project description:Pluripotent stem cells are increasingly used for therapeutic models, including transplantation of neural progenitors derived from human embryonic stem cells (hESCs). Recently, long non-coding RNAs (lncRNAs), including Maternally Expressed Gene 3 (MEG3) that is derived from DLK1-DIO3 imprinted locus, were found to be expressed during neural developmental events. Their deregulations are associated with various neurological diseases. The DLK1-DIO3 imprinted locus encodes abundant non-coding RNAs (ncRNAs) that are regulated by differential methylation on the locus. The aim of our research is to study the correlation between the DLK1-DIO3 derived ncRNAs and the capacity of hESC neural lineage differentiation. We classified hESCs into MEG3-ON and MEG3-OFF based on the expression levels of MEG3 as well as its downstream miRNAs by qRT-PCR. Initial embryoid body (EB) formation was conducted to examine the three germ layer differentiation ability. cDNA microarray was used to analyze the gene expression profiles of hESCs. Directed neural lineage differentiation was performed, followed by analysis of neural lineage marker expression levels and neurite formation via qRT-PCR and immunocytochemistry methods to investigate the capacity of neural differentiation in MEG3-ON and MEG3-OFF hESCs
2014-12-01 | GSE58508 | GEO
Project description:Pluripotent stem cells are increasingly used for therapeutic models, including transplantation of neural progenitors derived from human embryonic stem cells (hESCs). Recently, long non-coding RNAs (lncRNAs), including Maternally Expressed Gene 3 (MEG3) that is derived from DLK1-DIO3 imprinted locus, were found to be expressed during neural developmental events. Their deregulations are associated with various neurological diseases. The DLK1-DIO3 imprinted locus encodes abundant non-coding RNAs (ncRNAs) that are regulated by differential methylation on the locus. The aim of our research is to study the correlation between the DLK1-DIO3 derived ncRNAs and the capacity of hESC neural lineage differentiation. We classified hESCs into MEG3-ON and MEG3-OFF based on the expression levels of MEG3 as well as its downstream miRNAs by qRT-PCR. Initial embryoid body (EB) formation was conducted to examine the three germ layer differentiation ability. cDNA microarray was used to analyze the gene expression profiles of hESCs. Directed neural lineage differentiation was performed, followed by analysis of neural lineage marker expression levels and neurite formation via qRT-PCR and immunocytochemistry methods to investigate the capacity of neural differentiation in MEG3-ON and MEG3-OFF hESCs
2014-11-05 | GSE58809 | GEO
Project description:The molecular events during nongenotoxic carcinogenesis and their temporal order are poorly understood but thought to include long-lasting perturbations of gene expression. Here, we have investigated the temporal sequence of molecular and pathological perturbations at early stages of phenobarbital (PB) mediated liver tumor promotion in vivo. Molecular profiling (mRNA, microRNA [miRNA], DNA methylation, and proteins) of mouse liver during 13 weeks of PB treatment revealed progressive increases in hepatic expression of long noncoding RNAs and miRNAs originating from the Dlk1-Dio3 imprinted gene cluster, a locus that has recently been associated with stem cell pluripotency in mice and various neoplasms in humans. PB induction of the Dlk1-Dio3 cluster noncoding RNA (ncRNA) Meg3 was localized to glutamine synthetase-positive hypertrophic perivenous hepatocytes, sug- gesting a role for β-catenin signaling in the dysregulation of Dlk1-Dio3 ncRNAs. The carcinogenic relevance of Dlk1-Dio3 locus ncRNA induction was further supported by in vivo genetic dependence on constitutive androstane receptor and β-catenin pathways. Our data identify Dlk1-Dio3 ncRNAs as novel candidate early biomarkers for mouse liver tumor promotion and provide new opportunities for assessing the carcinogenic potential of novel compounds.
2016-04-08 | GSE80018 | GEO
Project description:Muscle-specific ablation of miR-1/133a expression leads to increased expression of miR-1/133a target genes at RNA and/or protein level. MEF2A is a direct target of miR-1/133a that is upregulated at the protein level and subsequently activates the expression of the Dlk1-Dio3 cluster in skeletal muscle of miR-1/133a deficient mice. miRNAs encoded in the Dlk1-Dio3 cluster directly repress the expression of multiple genes important for mitochondrial function. The study includes transcriptome analysis of tibialis anterior muscle after muscle-specific deletion of miR-1/133a as well as transcriptome analysis of tibialis anterior muscle after muscle-specific overexpression of Mef2A.
2018-03-30 | E-MTAB-5936 | biostudies-arrayexpress
Project description:Our previous study demonstrated a significant upregulation of a large set of miRNAs at the genomic imprinted Dlk1-Dio3 locus in lymphocytes of diverse murine lupus-prone strains. The upregulation of Dlk1-Dio3 miRNAs in lupus-prone mice is correlated with the global DNA hypomethylation. In this study, by performing genome-wide DNA methylation analysis, we reported that Dlk1-Dio3 genomic region in CD4+ T cells of MRL/lpr mice was hypomethylated, further linking hypomethylation to the increased expression of Dlk1-Dio3 miRNAs in lupus. Then, we assessed the gene expression levels of enzymes that either write (DNA methyltransferases, DNMTs) or erase DNA methylation (Ten-eleven translation proteins, TETs) to understand the molecular contributor to the DNA hypomethylation in MRL/lpr CD4+ T cells. The expression levels of Dnmt1, Dnmt3b, Tet1, and Tet2 were significantly increased in CD4+ T cells of MRL/lpr mice, as well as in B6/lpr and B6.sle123 mice, compared to their respective control mice. These data indicate the significant involvement of the TETs-mediated active demethylation pathway rather than reduced DNMTs-mediated passive demethylation pathway in the hypomethylation of murine lupus CD4+ T cells. The transcription factor, early growth response 2 (EGR2) is critically involved in regulating T cell functions and autoimmunity. In this research, we found that Egr2 deletion in B6/lpr mice notably reduced methylation-sensitive Dlk1-Dio3 cluster miRNAs expression in CD4+ T cells. Surprisingly, even though EGR2 has been shown to induce DNA demethylation by recruiting TET2, we found that deleting Egr2 in B6/lpr mice induced a higher number of hypomethylated DMRs than hypermethylated DMRs at either whole genome or the Dlk1-Dio3 locus in CD4+ T cells of B6/lpr mice. These data are the first finding on the positive role of EGR2 on the expression of Dlk1-Dio3 cluster miRNAs in lupus mice. Given that Dlk1-Dio3 miRNAs target the major signaling pathways in autoimmunity, these data provide a new perspective in understanding the potential pathogenic role of upregulated EGR2 in lupus.
2023-12-04 | GSE242955 | GEO
Project description:In placental mammals, adaptation to extra-uterine life requires complex metabolic adjustments linked to the abrupt transition from the transplacental transfer of glucose toward the use of fat originating from the motherM-bM-^@M-^Ys milk as a major energy source. The study of a novel knock-out mouse model led us to identify the biological roles of the miR-379/miR-410 cluster at the imprinted Dlk1-Dio3 region during this metabolic transition. The miR-379/miR-410 cluster is the largest mammalian-specific miRNA cluster composed of 39 pre-miRNA and expressed from the maternally-inherited allele. We unexpectedly found that ~ 35% of heterozygous neonates with a maternal - but not paternal - deletion of the entire 40kb-long miRNA cluster die shortly after birth due to defects in the maintenance of energy homeostasis, as evidenced by impaired hepatic glycogenolysis, gluconeogenesis and ketogenesis. This maladaptive metabolic response is accompanied by profound changes in the neonatal hepatic gene expression program, notably a decrease in the activation of a large set of metabolic genes linked to lipid metabolism. Our study unveils essential roles for the miR-379/miR-410 cluster at the transition from fetal to postnatal life, revealing new layers of RNA-mediated gene regulation at the Dlk1-Dio3 domain that impose parent-of-origin effects on postnatal metabolic functions. Liver gene expression was measured in mice with a maternally-inherited deletion of the miR-379/miR-410 cluster and in wild-type littermates at embryonic day E19.5, 4h following the caesarean delivery (n=4 biological replicates per genotype)
2014-08-22 | E-GEOD-47155 | biostudies-arrayexpress
Project description:In placental mammals, adaptation to extra-uterine life requires complex metabolic adjustments linked to the abrupt transition from the transplacental transfer of glucose toward the use of fat originating from the mother’s milk as a major energy source. The study of a novel knock-out mouse model led us to identify the biological roles of the miR-379/miR-410 cluster at the imprinted Dlk1-Dio3 region during this metabolic transition. The miR-379/miR-410 cluster is the largest mammalian-specific miRNA cluster composed of 39 pre-miRNA and expressed from the maternally-inherited allele. We unexpectedly found that ~ 35% of heterozygous neonates with a maternal - but not paternal - deletion of the entire 40kb-long miRNA cluster die shortly after birth due to defects in the maintenance of energy homeostasis, as evidenced by impaired hepatic glycogenolysis, gluconeogenesis and ketogenesis. This maladaptive metabolic response is accompanied by profound changes in the neonatal hepatic gene expression program, notably a decrease in the activation of a large set of metabolic genes linked to lipid metabolism. Our study unveils essential roles for the miR-379/miR-410 cluster at the transition from fetal to postnatal life, revealing new layers of RNA-mediated gene regulation at the Dlk1-Dio3 domain that impose parent-of-origin effects on postnatal metabolic functions.
2014-08-22 | GSE47155 | GEO
Project description:Imprinting at the Dlk1-Dio3 cluster is controlled by the IG-DMR, an imprinting control region differentially methylated between maternal and paternal chromosomes. The maternal IG-DMR is essential for imprinting control, functioning as a cis enhancer element. Meanwhile, DNA methylation at the paternal IG-DMR is thought to prevent enhancer activity. To explore whether suppression of enhancer activity at the methylated IG-DMR requires the transcriptional repressor TRIM28, we analyzed Trim28chatwo embryos and performed epistatic experiments with IG-DMR deletion mutants. We found that while TRIM28 regulates the enhancer properties of the paternal IG-DMR, it also controls imprinting through other mechanisms. Additionally, we found that the paternal IG-DMR, previously deemed dispensable for imprinting, is required in certain tissues, demonstrating that imprinting is regulated in a tissue-specific manner. Using ChRO-seq to analyze nascent transcription, we show that different tissues have a distinctive regulatory landscape at the Dlk1-Dio3 cluster, providing insight into potential mechanisms of tissue-specific imprinting control. ChRO-seq identified 30 novel transcribed regulatory elements, including a candidate regulatory region that depends on the paternal IG-DMR. Together, our findings challenge the model that Dlk1-Dio3 imprinting is regulated through a single mechanism and demonstrate that different tissues use distinct strategies for imprinting control.
2019-02-28 | GSE119882 | GEO