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Effect of TET deletion on the global DNA methylation status of osteoclasts

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE156130 | GEO | 2021/11/29

REPOSITORIES: GEO

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Effect of TET deletion on the global DNA methylation status of osteoclasts (RNA-Seq)

Project description:Epigenetic regulation is a fundamental mechanism mediating various cellular processes. However, epigenetic mechanisms in osteoclastogenesis remain incompletely understood. We performed RNA-seq analysis to investigate gene expression in osteoclasts derived from wild-type and Tet2Rank–/–; Tet3aRank+/– mice.

2021-11-29 | GSE156129 | GEO

Effect of TET deletion on the global DNA methylation status of osteoclasts (MeDIP-Seq)

Project description:Epigenetic regulation is a fundamental mechanism mediating various cellular processes. However, epigenetic mechanisms in osteoclastogenesis remain incompletely understood. We performed MeDIP-seq analysis to investigate DNA methylation in osteoclasts derived from wild-type and Tet2Rank–/–; Tet3aRank+/– mice.

2021-11-29 | GSE156128 | GEO

Effect of TET deletion on the global DNA methylation status of osteoclasts

Project description:Effect of TET deletion on the global DNA methylation status of osteoclasts

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Effect of Dnmt3a deletion on the global DNA methylation status of osteoclasts

Project description:Epigenetic regulation is a fundamental mechanism mediating various cellular processes. However, epigenetic mechanisms in osteoclastogenesis remain to be elucidated. We performed MBD-seq analysis to investigate DNA methylation in osteoclasts derived from wild-type and osteoclast-specific Dnmt3a knockout mice. Examination of DNA methylation in 2 cell types.

2015-02-23 | E-GEOD-59388 | biostudies-arrayexpress

Effect of Dnmt3a deletion on the global DNA methylation status of osteoclasts

Project description:Epigenetic regulation is a fundamental mechanism mediating various cellular processes. However, epigenetic mechanisms in osteoclastogenesis remain to be elucidated. We performed MBD-seq analysis to investigate DNA methylation in osteoclasts derived from wild-type and osteoclast-specific Dnmt3a knockout mice.

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Project description:Effect of TET deletion on the global DNA methylation status of osteoclasts (MeDIP-Seq)

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Project description:Effect of TET deletion on the global DNA methylation status of osteoclasts (RNA-Seq)

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Effect of Aid deletion on the global DNA methylation status of iPS cells

2014-04-10 | GSE52136 | GEO

Effect of Aid deletion on the global DNA methylation status of iPS cells

Project description:It has been shown that DNA demethylation has a pivotal role in the generation of induced pluripotent stem (iPS) cells. However, the underlying mechanism is still unclear. Previous reports indicated that activation-induced cytidine deaminase (Aid) is involved in DNA demethylation in several developmental processes and cell fusion-mediated reprogramming. Based on the reports, we hypothesized that Aid may be involved in DNA demethylation during the iPS cell generation. In this study, we examined the function of Aid in iPS cell generation using Aid knockout (Aid-/-) mice expressing a GFP reporter under the control of a pluripotent stem cell marker, Nanog. By the introduction of Oct3/4, Sox2, Klf4 and c-Myc, Nanog-GFP positive iPS cells could be generated from the fibroblasts and primary B cells of Aid-/- mice. The Aid-/- iPS cells showed normal proliferation and gave rise to chimeras, indicating their capacity for self-renewal and pluripotency. The comprehensive DNA methylation analysis by MBD-sequening demonstrated that there were only a few differences between Aid+/+ and Aid-/- iPS cells. Aid+/+ and Aid-/- iPS colonies were generated from Aid+/+ and Aid-/- MEFs and picked up mechanically. The clones were passaged four times on feeder cells and two times on gelatin-coated dishes to exclude the contamination of feeder cells. Subsequently, the genome was isolated. Four Aid+/+ iPS cell clones and four Aid-/- iPS cell clones were compared. To confirm the validity of MBD-sequencing, four Aid+/+ iPS cell clones were compared with three ES cell clones or three Aid+/+ MEFs.

2014-04-10 | E-GEOD-52136 | biostudies-arrayexpress

Effect of diabetes status and hyperglycemia on global DNA methylation and hydroxymethylation.

Project description:Type 2 diabetes mellitus (T2DM) is characterized by oxidative stress that could lead to chronic micro- and macrovascular complications. We hypothesized that some of the target organ damage is mediated by oxidative alterations in epigenetic mechanisms involving DNA methylation (5mC) and DNA hydroxymethylation (5hmC). We analyzed global DNA methylation and hydroxymethylation in peripheral blood cells in well-controlled and poorly controlled patients with T2DM and compared them with healthy controls. We also analyzed microarrays of DNA methylation and gene expression of other important tissues in the context of diabetes from the GEO database repository and then compared these results with our experimental gene expression data. DNA methylation and, more importantly, DNA hydroxymethylation levels were increased in poorly controlled patients compared to well-controlled and healthy individuals. Both 5mC and 5hmC measurements were correlated with the percentage of glycated hemoglobin, indicating a direct impact of hyperglycemia on changes over the epigenome. The analysis of methylation microarrays was concordant, and 5mC levels were increased in the peripheral blood of T2DM patients. However, the DNA methylation levels were the opposite of those in other tissues, such as the pancreas, adipose tissue and skeletal muscle. We hypothesize that a process of DNA oxidation associated with hyperglycemia may explain the DNA demethylation in which the activity of ten-eleven translocation (TET) proteins is not sufficient to complete the process. High levels of glucose lead to cellular oxidation, which triggers the process of DNA demethylation aided by TET enzymes, resulting in epigenetic dysregulation of the damaged tissues.

| S-EPMC5670276 | biostudies-literature

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