Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Vitamin C promotes epidermal proliferation by enhancing the DNA demethylation of proliferation-related genes in human epidermal equivalents (WGBS)

ABSTRACT: The stratified structure of the epidermis, the outermost layer of the skin, is highly regulated through the differentiation of keratinocytes. Vitamin C act as a cofactor for DNA demethylation enzyme ten-eleven translocation (TET) in epigenetic mechanism. Previous study revealed that VC deficiency causes epidermal atrophy in hairless mice unable to synthesize VC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE273778 | GEO | 2025/04/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Vitamin C promotes epidermal proliferation by enhancing the DNA demethylation of proliferation-related genes in human epidermal equivalents (Microarray)

Project description:The stratified structure of the epidermis, the outermost layer of the skin, is highly regulated through the differentiation of keratinocytes. Vitamin C act as a cofactor for DNA demethylation enzyme ten-eleven translocation (TET) in epigenetic mechanism. Previous study revealed that VC deficiency causes epidermal atrophy in hairless mice unable to synthesize VC. We used microarrays to examine in detail the differences in gene expression in keratinocytes with and without VC addition.

2025-04-09 | GSE274382 | GEO

Vitamin C promotes epidermal proliferation by enhancing the DNA demethylation of proliferation-related genes in human epidermal equivalents (WGBS)

Project description:Vitamin C promotes epidermal proliferation by enhancing the DNA demethylation of proliferation-related genes in human epidermal equivalents (WGBS)

| PRJNA1143040 | ENA

Vitamin C promotes epidermal proliferation by enhancing the DNA demethylation of proliferation-related genes in human epidermal equivalents (Microarray)

Project description:Vitamin C promotes epidermal proliferation by enhancing the DNA demethylation of proliferation-related genes in human epidermal equivalents (Microarray)

| PRJNA1146319 | ENA

Vitamin C dependent KDM6 demethylation specifies a functional chromatin state for endothelial-to-hematopoietic transition [RNA-Seq]

Project description:Hematopoietic stem/progenitor cells (HSPCs) are generated from hemogenic endothelial cells (HECs) through endothelial-to-hematopoietic transition (EHT); however, the underlying mechanism remains poorly understood. Here, we report that HPC generation is significantly reduced in hPSC differentiatiation in a defined condition without vitamin C (Vc). Mechanistically, the endothelial cells generated in the absence of Vc fail to undergo EHT due to apparent failure in opening genomic loci essential for hematopoiesis. These loci exhibit abnormal accumulation of H3K27me3, a repressive histone modification due to lower activity of its demethylases. Consistently, deletion of H3K27me3 demethylases, JMJD3 and UTX, impaires HPC generation in the presence of Vc. Furthermore, Vc and jmjd3 are also important for HSC generation during zebrafish development. Together, we reveal an obligatory role of Vc underlying EHT process in hematopoisis and further support the important function of Vc during development.

2019-07-22 | GSE132969 | GEO

Vitamin C dependent KDM6 demethylation specifies a functional chromatin state for endothelial-to-hematopoietic transition [ChIP-Seq]

2019-07-22 | GSE132834 | GEO

Natural depletion of H1 in sex cells causes DNA demethylation, heterochromatin decondensation and transposon activation

Project description:Transposable elements (TEs) are largely inactive. Interestingly, a subset of TEs are naturally expressed in the vegetative cell (VC) of the male gametophyte, pollen in Arabidopsis. However, the extent and mechanism of such TE activation were unknown. Through RNA-seq, we identified pollen-activated TEs and annotated the transcriptional start sites (TSSs) and transcriptional termination sites (TTSs) using a program called Mikado. We have previously shown that H1 is expressed in sperm but not in VC, which prompted us to ectopically express H1 in VC for studying TE regulation through RNA-seq and bisulfite-seq. Our RNA-seq data shows that H1 expression in VC represses some of pollen-activated TEs. Furthermore, bisulfite-seq data from the pollen nuclei isolated via fluorescence-activated cell sorting (FACS) shows that H1 expression in VC increases DNA methylation of some of H1-repressed TEs around their TSSs, while leaving other H1-repressed TEs unchanged in DNA methylation. Our results indicate that H1 represses TE expression through both DNA methylation-dependent and -independent mechanisms and that natural depletion of H1 in VC allows TEs to be activated.

2019-05-29 | GSE120519 | GEO

Lowered humidity produces human epidermal equivalents with enhanced barrier properties.

Project description:Multilayered human keratinocyte cultures increasingly are used to model human epidermis. Until now, studies utilizing human epidermal equivalents (HEEs) have been limited because previous preparations do not establish a normal epidermal permeability barrier. In this report, we show that reducing environmental humidity to 50% relative humidity yields HEEs that closely match human postnatal epidermis and have enhanced repair of the permeability barrier. These cultures display low transepidermal water loss and possess a calcium and pH gradient that resembles those seen in human epidermis. These cultures upregulate glucosylceramide synthase and make normal-appearing lipid lamellar bilayers. The epidermal permeability barrier of these cultures can be perturbed, using the identical tools previously described for human skin, and recover in the same time course seen during in vivo barrier recovery. These cultures will be useful for basic and applied studies on epidermal barrier function.

| S-EPMC4291214 | biostudies-literature

Vitamin C-dependent lysine demethylase 6 (KDM6)-mediated demethylation promotes a chromatin state that supports the endothelial-to-hematopoietic transition

Project description:Hematopoietic stem cells (HSCs)/progenitor cells (HPCs) are generated from hemogenic endothelial cells (HECs) during the endothelial-to-hematopoietic transition (EHT); however, the underlying mechanism remains poorly understood. Here, using an array of approaches, including CRSPR/Cas9 gene knockouts, RNA-Seq, ChIP-Seq, ATAC-Seq etc., we report that vitamin C (Vc) is essential in HPC generation during human pluripotent stem cell (hPSC) differentiation in defined culture conditions. Mechanistically, we found that the endothelial cells generated in the absence of Vc fail to undergo the EHT because of an apparent failure in opening up genomic loci essential for hematopoiesis. Under Vc deficiency, these loci exhibited abnormal accumulation of histone H3 trimethylation at Lys-27 (H3K27me3), a repressive histone modification that arose because of lower activities of demethylases that target H3K27me3. Consistently, deletion of the two H3K27me3 demethylases, Jumonji domain-containing 3 (JMJD3 or KDM6B) and histone demethylase UTX (UTX or KDM6A), impaired HPC generation even in the presence of Vc. Furthermore, we noted that Vc and jmjd3 are also important for HSC generation during zebrafish development. Together, our findings reveal an essential role for Vc in the EHT for hematopoiesis, and identify KDM6-mediated chromatin demethylation as an important regulatory mechanism in hematopoietic cell differentiation.

2019-07-22 | GSE132833 | GEO

Long noncoding RNA FENDRR inhibits lung fibroblast proliferation via a reduction of beta-catenin

Project description:Adenovirus-mediated FENDRR transfer to the lungs of mice reduced asbestos-induced fibrotic lesions and collagen deposition.RNA sequencing analysis was used to profile the gene expression in the lungs of asbestos-treated (VC-Cro) mice compared to control (VC-TiO2).

2021-05-26 | GSE175496 | GEO

Enhancing demethylation-induced differentiation in IDH-mutant glioma.

Project description: Not available

| S-EPMC9071324 | biostudies-literature