Ten-Eleven Translocation 1 and 2 Confer Overlapping Transcriptional Programs for the Proliferation of Cultured Adult Neural Stem Cells

Shimozaki, Koji

doi:10.1007/s10571-016-0432-6

Cited by 7 publications

(8 citation statements)

References 76 publications

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“…It has been reported that P16 INK4a affects cell proliferation and differentiation by negatively regulating the cell cycle (32). Recently, several studies have reported that TET2 regulates cell cycle-associated proteins in neural and trophoblast stem cells (28,29). In line with these previous studies, the results of the present study suggested that the increase in P16 INK4a expression was mediated by TET2 overexpression, and si-TET2 decreased the level of P16 INK4a expression.…”

Section: Discussionsupporting

confidence: 89%

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TET2 is involved in DNA hydroxymethylation, cell proliferation and inflammatory response in keratinocytes

et al. 2020

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dna methylation and hydroxymethylation are the most common epigenetic modifications associated with the cell cycle and the inflammatory response. The present study aimed to investigate the role of 5-hydroxymethyl-cytosine (5-hmc) and ten-eleven translocation-2 (TET2) in keratinocytes. Following TET2 knockdown, dot blot analysis was performed to assess the levels of 5-hmC in keratinocytes, using HaCaT cells. Subsequently, the viability and cell cycle of HaCaT cells were assessed by MTT, Cell Counting Kit-8 assay and flow cytometric assays. Cyclin-dependent kinase inhibitor 2A and proinflammatory cytokine protein and mrna expression levels were also detected. The present results suggested that TET2 may play an important role in regulating cellular proliferation by mediating DNA hydroxymethylation in HaCaT cells. In addition, TET2 knockdown decreased the production of proinflammatory cytokines, including lipocalin 2, S100 calcium binding protein A7, matrix metallopeptidase 9, C-X-C motif chemokine ligand 1, interferon regulatory factor 7 and interleukin-7 receptor. The present study suggested that TET2 regulated cell viability, apoptosis and the expression of inflammatory mediators in keratinocytes. Collectively, the results indicated that TET2 knockdown may relieve inflammatory responses in the skin.

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Section: Discussionsupporting

confidence: 89%

“…TET2 affects cellular proliferation and cell cycle progression in various cell lines, such as CD4 + T and Hela cells, in other conditions, including autoimmune diseases and development (5,(27)(28)(29)(30). However, the precise mechanism underlying TET2 in HaCaT cells remains unclear.…”

Section: Discussionmentioning

confidence: 99%

TET2 is involved in DNA hydroxymethylation, cell proliferation and inflammatory response in keratinocytes

et al. 2020

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“…This also implies that centrosome defects alone do not explain the slower proliferation rates and increased frequency of endoreduplication. A previous study showed that both TET1 and TET2 regulate the transcription of genes related to DNA replication (e.g., Mcm2/3/4/5/6 ) and cell-cycle progression (e.g., Ccne1 , Md2l1 , and E2f2 ) in neural stem cells ( Shimozaki, 2017 ). We also observe TET1 enrichment at cell-cycle gene loci where it likely serves to maintain an open, active chromatin configuration, akin to our findings at the Cdh1 locus.…”

Section: Discussionmentioning

confidence: 99%

A Critical Role of TET1/2 Proteins in Cell-Cycle Progression of Trophoblast Stem Cells

et al. 2018

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SummaryThe ten-eleven translocation (TET) proteins are well known for their role in maintaining naive pluripotency of embryonic stem cells. Here, we demonstrate that, jointly, TET1 and TET2 also safeguard the self-renewal potential of trophoblast stem cells (TSCs) and have partially redundant roles in maintaining the epithelial integrity of TSCs. For the more abundantly expressed TET1, we show that this is achieved by binding to critical epithelial genes, notably E-cadherin, which becomes hyper-methylated and downregulated in the absence of TET1. The epithelial-to-mesenchymal transition phenotype of mutant TSCs is accompanied by centrosome duplication and separation defects. Moreover, we identify a role of TET1 in maintaining cyclin B1 stability, thereby acting as facilitator of mitotic cell-cycle progression. As a result, Tet1/2 mutant TSCs are prone to undergo endoreduplicative cell cycles leading to the formation of polyploid trophoblast giant cells. Taken together, our data reveal essential functions of TET proteins in the trophoblast lineage.

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“…This group of enzymes are dependent on the TCA cycle metabolite α-ketoglutarate and oxygen as essential substrates and Fe 2+ as an essential co-factor [96]. TET1 and TET2 have overlapping functions [97], a level of redundancy that reflects their biological importance, whilst TET3 is thought to be important during reprogramming within the oocyte [98] although it has recently been shown to be important at later developmental stages within the retina [99]. The TET enzymes can be regulated at multiple levels, including through DNA methylation at the TET1 and TET2 promoters [100, 101], through the action of transcription factors such as HIF1β [102], and through regulation at the mRNA and protein level [103-107].…”

Section: Epigenetic Modificationsmentioning

confidence: 99%

Preterm Birth and the Risk of Neurodevelopmental Disorders - Is There a Role for Epigenetic Dysregulation?

Fitzgerald

Boardman

Drake

2018

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Preterm Birth (PTB) accounts for approximately 11% of all births worldwide each year and is a profound physiological stressor in early life. The burden of neuropsychiatric and developmental impairment is high, with severity and prevalence correlated with gestational age at delivery. PTB is a major risk factor for the development of cerebral palsy, lower educational attainment and deficits in cognitive functioning, and individuals born preterm have higher rates of schizophrenia, autistic spectrum disorder and attention deficit/hyperactivity disorder. Factors such as gestational age at birth, systemic inflammation, respiratory morbidity, sub-optimal nutrition, and genetic vulnerability are associated with poor outcome after preterm birth, but the mechanisms linking these factors to adverse long term outcome are poorly understood. One potential mechanism linking PTB with neurodevelopmental effects is changes in the epigenome. Epigenetic processes can be defined as those leading to altered gene expression in the absence of a change in the underlying DNA sequence and include DNA methylation/hydroxymethylation and histone modifications. Such epigenetic modifications may be susceptible to environmental stimuli, and changes may persist long after the stimulus has ceased, providing a mechanism to explain the long-term consequences of acute exposures in early life. Many factors such as inflammation, fluctuating oxygenation and excitotoxicity which are known factors in PTB related brain injury, have also been implicated in epigenetic dysfunction. In this review, we will discuss the potential role of epigenetic dysregulation in mediating the effects of PTB on neurodevelopmental outcome, with specific emphasis on DNA methylation and the α-ketoglutarate dependent dioxygenase family of enzymes.

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Ten-Eleven Translocation 1 and 2 Confer Overlapping Transcriptional Programs for the Proliferation of Cultured Adult Neural Stem Cells

Cited by 7 publications

References 76 publications

TET2 is involved in DNA hydroxymethylation, cell proliferation and inflammatory response in keratinocytes

TET2 is involved in DNA hydroxymethylation, cell proliferation and inflammatory response in keratinocytes

A Critical Role of TET1/2 Proteins in Cell-Cycle Progression of Trophoblast Stem Cells

Preterm Birth and the Risk of Neurodevelopmental Disorders - Is There a Role for Epigenetic Dysregulation?

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