Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Vitamin C enhances NF-κB-driven DNA demethylation and immunogenic properties of dendritic cells

ABSTRACT: Vitamin C enhances NF-κB-driven DNA demethylation and immunogenic properties of dendritic cells

PROVIDER: PRJNA840900 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19333078_1.fastq.gz	Fastqsanger.gz
	SRR19333078_2.fastq.gz	Fastqsanger.gz
	SRR19333079_1.fastq.gz	Fastqsanger.gz
	SRR19333079_2.fastq.gz	Fastqsanger.gz
	SRR19333080_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 42

Similar Datasets

Vitamin C enhances NF-κB-driven DNA demethylation and immunogenic properties of dendritic cells [methylation II]

Project description:Dendritic cells (DCs) are central in immune responses, bridging the adaptive and innate systems. The study of the in vitro differentiation of DCs from monocytes provides both an in-depth understanding of the analogous in vivo process and a potential source for cancer cell therapy. Active DNA demethylation has been previously reported to be crucial in DC differentiation. Vitamin C, an essential nutrient, is a known cofactor of ten-eleven translocation (TET) enzymes, which drive active demethylation. Currently, the effects of vitamin C treatment on human immune cells are poorly understood. In this study, we have analyzed the epigenomic and transcriptomic reprogramming orchestrated by vitamin C in monocyte-derived DC differentiation and maturation. We have detected extensive demethylation produced by vitamin C treatment, together with concordant gene expression changes during DC maturation. p65, a component of NF-kB, interacts with TET2 and produces both vitamin C-mediated gene upregulation and DNA demethylation during DC maturation, as demonstrated by chemical inhibition. Moreover, vitamin C increases TNFβ production in DCs through p65, in concordance with the upregulation of its coding gene and DNA demethylation of adjacent CpGs. Finally, vitamin C increases DC's ability to stimulate the proliferation of autologous antigen-specific T cells. This work provides a potential strategy for the improvement of cell therapies based on monocyte-derived DCs, as well as a feasible mechanism of action for intravenous high-dose vitamin C treatment in patients.

2022-10-06 | GSE213040 | GEO

Vitamin C enhances NF-κB-driven DNA demethylation and immunogenic properties of dendritic cells [RNA-Seq]

2022-10-06 | GSE203460 | GEO

Vitamin C enhances NF-κB-driven DNA demethylation and immunogenic properties of dendritic cells [RNA-Seq]

Project description:Vitamin C enhances NF-κB-driven DNA demethylation and immunogenic properties of dendritic cells [RNA-Seq]

| PRJNA840904 | ENA

Vitamin C enhances NF-κB-driven DNA demethylation and immunogenic properties of dendritic cells [methylation II]

Project description:Vitamin C enhances NF-κB-driven DNA demethylation and immunogenic properties of dendritic cells [methylation II]

| PRJNA878818 | ENA

Vitamin C enhances NF-?B-driven DNA demethylation and immunogenic properties of dendritic cells [methylation I]

2022-10-06 | GSE203461 | GEO

Vitamin C enhances NF-?B-driven DNA demethylation and immunogenic properties of dendritic cells [methylation I]

Project description:Vitamin C enhances NF-?B-driven DNA demethylation and immunogenic properties of dendritic cells [methylation I]

| PRJNA840903 | ENA

Vitamin C enhances NF-κB-driven DNA demethylation and immunogenic properties of dendritic cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-10-06 | GSE203463 | GEO

Vitamin C Induces Specific Demethylation of H3K9me2 in Mouse Embryonic Stem Cells via Kdm3a/b

Project description:Histone methylation patterns regulate gene expression and are highly dynamic during development. The erasure of histone methylation is carried out by histone demethylase enzymes. We had previously shown that vitamin C enhances the activity of Tet enzymes in embryonic stem (ES) cells, leading to DNA demethylation and activation of germline genes. We report here that vitamin C induces a remarkably specific demethylation of histone H3 lysine 9 dimethylation (H3K9me2) in ES cells. Vitamin C treatment reduces global levels of H3K9me2, but not other histone methylation marks analyzed, as measured by Western blot, immunofluorescence and mass spectrometry. Vitamin C leads to widespread loss of H3K9me2 at large chromosomal domains as well as gene promoters and repeat elements. Vitamin C-induced loss of H3K9me2 occurs rapidly within 24 hours and is reversible. Importantly, we found that the histone demethylases Kdm3a and Kdm3b are required for vitamin C-induced demethylation of H3K9me2. Moreover, we show that vitamin C-induced Kdm3a/b-mediated H3K9me2 demethylation and Tet-mediated DNA demethylation are independent processes. Lastly, we document Kdm3a/b are partially required for the up-regulation of germline genes by vitamin C. These results reveal a specific role for vitamin C in histone demethylation in ES cells, and document that DNA methylation and H3K9me2 cooperate to silence germline genes in pluripotent cells.

2017-06-30 | GSE84009 | GEO

Maternal Vitamin C regulates DNA demethylation and development of the mouse embryonic germline [RRBS]

Project description:Maternal Vitamin C is required in vivo for proper DNA demethylation and development of fetal germ cells in a mouse model of Vitamin C deficiency. Withdrawal of Vitamin C from the maternal diet does not affect overall embryonic development but leads to defects in the fetal germline, which persist well after Vitamin C re-supply during late gestation. The transcriptome of germ cells from Vitamin C-deficient embryos is remarkably similar to that of embryos carrying a mutation in Tet1, which is responsible for DNA demethylation and activation of regulators of meiosis. In agreement with these results, Vitamin C deficiency leads to an aberrant DNA methylation profile that includes incomplete demethylation of key regulators of meiosis and transposable elements. These findings reveal that deficiency in Vitamin C during gestation recapitulates a mutation in Tet1 and disrupts germline reprogramming and development. Our work further indicate that the embryonic germline is sensitive to perturbations of the maternal diet, providing a potential intergenerational mechanism for adjusting fecundity to environmental quality.

2019-07-01 | GSE109746 | GEO

Vitamin C enhances NF-κB-driven epigenomic reprogramming and boosts the immunogenic properties of dendritic cells.

Project description:Dendritic cells (DCs), the most potent antigen-presenting cells, are necessary for effective activation of naïve T cells. DCs' immunological properties are modulated in response to various stimuli. Active DNA demethylation is crucial for DC differentiation and function. Vitamin C, a known cofactor of ten-eleven translocation (TET) enzymes, drives active demethylation. Vitamin C has recently emerged as a promising adjuvant for several types of cancer; however, its effects on human immune cells are poorly understood. In this study, we investigate the epigenomic and transcriptomic reprogramming orchestrated by vitamin C in monocyte-derived DC differentiation and maturation. Vitamin C triggers extensive demethylation at NF-κB/p65 binding sites, together with concordant upregulation of antigen-presentation and immune response-related genes during DC maturation. p65 interacts with TET2 and mediates the aforementioned vitamin C-mediated changes, as demonstrated by pharmacological inhibition. Moreover, vitamin C increases TNFβ production in DCs through NF-κB, in concordance with the upregulation of its coding gene and the demethylation of adjacent CpGs. Finally, vitamin C enhances DC's ability to stimulate the proliferation of autologous antigen-specific T cells. We propose that vitamin C could potentially improve monocyte-derived DC-based cell therapies.

| S-EPMC9638940 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data