scholarly journals DNA methylation and its role in the trophoblast cell lineage

2014 ◽  
Vol 58 (2-3-4) ◽  
pp. 231-238 ◽  
Author(s):  
Satoshi Tanaka ◽  
Momo O. Nakanishi ◽  
Kunio Shiota
Keyword(s):  
Dna Methylation ◽  
Cell Lineage ◽  
Trophoblast Cell

scholarly journals Accounting for cell lineage and sex effects in the identification of cell-specific DNA methylation using a Bayesian model selection algorithm

PLoS ONE ◽  
2017 ◽  
Vol 12 (9) ◽  
pp. e0182455 ◽  
Author(s):  
Nicole White ◽  
Miles Benton ◽  
Daniel Kennedy ◽  
Andrew Fox ◽  
Lyn Griffiths ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Model Selection ◽  
Bayesian Model ◽  
Cell Lineage ◽  
Bayesian Model Selection ◽  
Selection Algorithm ◽  
Sex Effects

scholarly journals Differential DNA Methylation in Purified Human Blood Cells: Implications for Cell Lineage and Studies on Disease Susceptibility

PLoS ONE ◽  
2012 ◽  
Vol 7 (7) ◽  
pp. e41361 ◽  
Author(s):  
Lovisa E. Reinius ◽  
Nathalie Acevedo ◽  
Maaike Joerink ◽  
Göran Pershagen ◽  
Sven-Erik Dahlén ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Human Blood ◽  
Blood Cells ◽  
Disease Susceptibility ◽  
Cell Lineage ◽  
Human Blood Cells

Dynamic Regulation of the Chromatin Landscape during Human Extravillous Trophoblast Cell Lineage Development

Placenta ◽  
2021 ◽  
Vol 112 ◽  
pp. e16-e17
Author(s):  
Kaela M. Varberg ◽  
Boryana Koseva ◽  
Khursheed Iqbal ◽  
Jinchu Vijay ◽  
Rebecca Biswell ◽  
...  
Keyword(s):  
Cell Lineage ◽  
Trophoblast Cell ◽  
Extravillous Trophoblast ◽  
Dynamic Regulation

Exogenous CRIPTO-1 increases proliferation of the trophoblast cell lineage HTR8/SV-neo

Placenta ◽  
2019 ◽  
Vol 83 ◽  
pp. e118
Author(s):  
Milena Mirandola ◽  
Jady Rabelo ◽  
Carla Bandeira ◽  
Marco Amadeu ◽  
Estela Bevilacqua
Keyword(s):  
Cell Lineage ◽  
Trophoblast Cell

Homeobox gene HB24, a regulator of haematopoiesis, is a candidate for regulating differentiation of the extra-embryonic trophoblast cell lineage

1997 ◽  
Vol 9 (6) ◽  
pp. 617 ◽  
Author(s):  
L. M. Quinn ◽  
S. E. Latham ◽  
B. Kalionis
Keyword(s):  
Cell Lineage ◽  
Homeobox Gene ◽  
Trophoblast Cell ◽  
Northern Analysis ◽  
Stem Cell Population ◽  
Term Placenta ◽  
Haematopoietic Cell ◽  
Cytotrophoblast Cells ◽  
Ribonuclease Protection ◽  
Extravillous Cytotrophoblast

Expression of the human homeobox gene HB24 in the cytotrophoblast stem cell population in rst-trimester human placenta was investigated. HB24expression was downregulated after cytotrophoblast had differentiated into syncytiotrophoblast. Expression of HB24 was also detected in rst-trimester invasive extravillous cytotrophoblast cells. In term placenta, HB24 expression was detected in residual cytotrophoblast cells and in syncytiotrophoblast. Northern analysis revealed two HB24 transcripts in rst-trimester placenta of approximately 2·5 kb and 5·3 kb. Ribonuclease protection assays were used to conrm expression of HB24 in rst-trimester and term placenta and also to provide evidence that HB24 is downregulated in choriocarcinoma cell lines. In addition to being required for differentiation of the haematopoietic cell lineage, HB24 may be required for differentiation of the extra-embryonic trophoblast cell lineage.

PI3K/AKT SIGNALING REGULATES HUMAN EXTRAVILLOUS TROPHOBLAST CELL LINEAGE DEVELOPMENT

Placenta ◽  
2021 ◽  
Vol 112 ◽  
pp. e53-e54
Author(s):  
Keisuke Kozai ◽  
Vinay Shukla ◽  
Michael J. Soares
Keyword(s):  
Cell Lineage ◽  
Akt Signaling ◽  
Trophoblast Cell ◽  
Extravillous Trophoblast

scholarly journals DNA Methylation-based Signatures Classify Sporadic Pituitary Tumors According to Clinicopathological Features

2020 ◽  
Author(s):  
Maritza S. Mosella ◽  
Thais S. Sabedot ◽  
Tiago C. Silva ◽  
Tathiane M. Malta ◽  
Felipe D. Segato ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Functional Status ◽  
Cell Lineage ◽  
Pituitary Tumors ◽  
Clinicopathological Features ◽  
List Type ◽  
Cell Identity ◽  
Cell Lineages ◽  
Adenohypophyseal Cell ◽  
Recent Classification

ABSTRACTBackgroundDistinct genome-wide methylation patterns have consistently clustered pituitary neuroendocrine tumors (PT) into molecular groups associated with specific clinicopathological features. Here we aim to identify, characterize and validate the methylation signatures that objectively classify PT into those molecular groups.MethodsCombining in-house and publicly available data, we conducted an analysis of the methylome profile of a comprehensive cohort of 177 tumor and 20 non-tumor specimens from the pituitary gland. We also retrieved methylome data from an independent pituitary tumor (PT) cohort (N=86) to validate our findings.ResultsWe identified three methylation clusters associated with functional status and adenohypophyseal cell lineages using an unsupervised approach. We also identified signatures based on differentially methylated CpG probes (DMP), some of which overlapped with pituitary-specific transcription factors genes (SF1 and Tpit), that significantly distinguished pairs of clusters related to functional status and adenohypophyseal cell lineage. These findings were reproduced in an independent cohort, validating these methylation signatures. The DMPs were mainly annotated in enhancer regions associated with pathways and genes involved in cell identity and tumorigenesis.ConclusionsWe identified and validated methylation signatures that distinguished PT by distinct functional status and adenohypophyseal cell lineages. These signatures, annotated in enhancer regions, indicate the importance of these elements in pituitary tumorigenesis. They also provide an unbiased approach to classify pituitary tumors according to the most recent classification recommended by the WHO 2017 using methylation profiling.Key-pointsDistinct methylation landscapes define PT groups with specific functional status/subtypes and adenohypophyseal lineages subtypes.Methylation abnormalities in each cluster mainly occur in CpG annotated in distal regions overlapping predicted enhancers regions associated with pathways and genes involved in cell identity and tumorigenesis.DNA methylation signatures provide an unbiased approach to classify PT.Importance of the studyThis study harnessed the largest methylome data to date from a comprehensive cohort of pituitary specimens obtained from four different institutions. We identified and validated methylation signatures that distinguished pituitary tumors into molecular groups that reflect the functionality and adenohypophyseal cell lineages of these tumors. These signatures, mainly located in enhancers, are associated with pathways and genes involved in cell identity and tumorigenesis. Our results show that methylome profiling provides an objective approach to classify PT according to the most recent classification of PT recommended by the 2017 WHO.

Effects of 5-azacytidine on methylation and expression of specific DNA sequences in C3H 10T1/2 cells

1984 ◽  
Vol 4 (4) ◽  
pp. 634-641
Author(s):  
W L Hsiao ◽  
S Gattoni-Celli ◽  
P Kirschmeier ◽  
I B Weinstein
Keyword(s):  
Dna Methylation ◽  
Dna Sequences ◽  
Cell Lineage ◽  
Population Level ◽  
Restriction Enzymes ◽  
Detectable Level ◽  
Beta Globin ◽  
Mouse Embryo Fibroblasts ◽  
Per Se ◽  
Differential Digestion

The present study indicates that the transient exposure of C3H 10T1/2 mouse embryo fibroblasts to 5-azacytidine leads to extensive loss of methylation of the protooncogene c-mos and the beta-globin locus at the cell population level and in at least 40 isolated subclones. These changes persisted, even when the cells were serially passaged for many generations without further exposure to the drug. Even though the amount of demethylation, assessed through differential digestion by the restriction enzymes HpaII and MspI, was quite extensive, neither locus was transcribed at a detectable level. This nonselective analysis suggests, therefore, that loss of DNA methylation is not sufficient per se to induce the expression of certain loci. Presumably, the expression of these loci requires additional factors, some of which may be related to cell lineage and differentiation.

The role of the mtDNA set point in differentiation, development and tumorigenesis

2016 ◽  
Vol 473 (19) ◽  
pp. 2955-2971 ◽  
Author(s):  
Xin Sun ◽  
Justin C. St. John
Keyword(s):  
Dna Methylation ◽  
Cell Fate ◽  
Copy Number ◽  
Developmental Disorders ◽  
Cell Lineage ◽  
Mtdna Copy Number ◽  
Exon 2 ◽  
Set Point ◽  
Dna Polymerase Gamma ◽  
Key Factor

Mitochondrial DNA replication is critical for maintaining mtDNA copy number to generate sufficient cellular energy that is required for development and for functional cells. In early development, mtDNA copy number is strictly regulated at different stages, and, as a result, the establishment of the mtDNA set point is required for sequential cell lineage commitment. The failure to establish the mtDNA set point results in incomplete differentiation or embryonic arrest. The regulation of mtDNA copy number during differentiation is closely associated with cellular gene expression, especially with the pluripotency network, and DNA methylation profiles. The findings from cancer research highlight the relationship between mitochondrial function, mtDNA copy number and DNA methylation in regulating differentiation. DNA methylation at exon 2 of DNA polymerase gamma subunit A (POLGA) has been shown to be a key factor, which can be modulated to change the mtDNA copy number and cell fate of differentiating and tumour cells. The present review combines multi-disciplinary data from mitochondria, development, epigenetics and tumorigenesis, which could provide novel insights for further research, especially for developmental disorders and cancers.

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