Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (single cell RNA-Seq)

ABSTRACT: Unbiased whole-genome methylome was studied in the wound-edge (WE) tissue of chronic wound patients. Methylation status of proximal promoter (1Kb) was calculated using MethylCap-Seq and PrEMeR-CG data analyses. A total of 4689 differentially methylated regions (DMRs) were identified in chronic WE compared to unwounded (UW) human skin. Hypermethylation was more frequently observed (3661 DMRs) in the chronic WE compared to hypomethylation (1028 DMRs). Twenty-six hypermethylated DMRs were involved in epithelial to mesenchymal transition (EMT). Bisulfite sequencing validated hypermethylation of a predicted specific upstream regulator TP53. Whole genome RNA sequencing analysis was performed to qualify findings from methylome analysis. Hierarchical clustering analyses identified a large set of genes, the expression of which were significantly downregulated in chronic WE compared to UW skin. Analysis of the downregulated genes identified the TP53 signaling pathway, including P63, P73, FOXO3, SIRT1 and HDAC1, as being significantly silenced. Direct comparison of hypermethylation and downregulated gene expression identified four genes, ADAM17, NOTCH, TWIST1 and SMURF1, that were common to both data sets and functionally represented the EMT pathway. Single cell RNA sequencing studies identified that these effects on gene expression were limited to the keratinocyte cell compartment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE176415 | GEO | 2022/05/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (MethylCap-seq)

Project description:Unbiased whole-genome methylome was studied in the wound-edge (WE) tissue of chronic wound patients. Methylation status of proximal promoter (1Kb) was calculated using MethylCap-Seq and PrEMeR-CG data analyses. A total of 4689 differentially methylated regions (DMRs) were identified in chronic WE compared to unwounded (UW) human skin. Hypermethylation was more frequently observed (3661 DMRs) in the chronic WE compared to hypomethylation (1028 DMRs). Twenty-six hypermethylated DMRs were involved in epithelial to mesenchymal transition (EMT). Bisulfite sequencing validated hypermethylation of a predicted specific upstream regulator TP53. Whole genome RNA sequencing analysis was performed to qualify findings from methylome analysis. Hierarchical clustering analyses identified a large set of genes, the expression of which were significantly downregulated in chronic WE compared to UW skin. Analysis of the downregulated genes identified the TP53 signaling pathway, including P63, P73, FOXO3, SIRT1 and HDAC1, as being significantly silenced. Direct comparison of hypermethylation and downregulated gene expression identified four genes, ADAM17, NOTCH, TWIST1 and SMURF1, that were common to both data sets and functionally represented the EMT pathway. Single cell RNA sequencing studies identified that these effects on gene expression were limited to the keratinocyte cell compartment.

2022-05-04 | GSE176413 | GEO

Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (RNA-Seq)

2022-05-04 | GSE176414 | GEO

Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (Spatial RNA-Seq)

2022-05-04 | GSE176416 | GEO

Enhanced epigenetic profiling of classical human monocytes reveals a specific signature of healthy aging in the DNA methylome

Project description:The impact of healthy aging on molecular programming of immune cells is poorly understood. Here, we report comprehensive characterization of healthy aging in human classical monocytes, with a focus on epigenomic, transcriptomic, and proteomic alterations, as well as the corresponding proteomic and metabolomic data for plasma, using healthy cohorts of 20 young and 20 older males (~27 and ~64 years old on average). For each individual, we performed eRRBS-based DNA methylation profiling, which allowed us to identify a set of age-associated differentially methylated regions (DMRs) – a novel, cell-type specific signature of aging in DNA methylome. Hypermethylation events were associated with H3K27me3 in the CpG islands near promoters of lowly-expressed genes, while hypomethylated DMRs were enriched in H3K4me1 marked regions and associated with age-related increase of expression of the corresponding genes, providing a link between DNA methylation and age-associated transcriptional changes in primary human cells.

2022-02-16 | PXD021821 | Pride

Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition

Project description:Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition

| PRJNA736091 | ENA

Metabolic Reprogramming and Reliance in Human Skin Wound Healing

Project description:Impaired skin wound healing is a significant global health issue, especially among the elderly. Wound healing is a well-orchestrated process involving the sequential phases of inflammation, proliferation, and tissue remodeling. Although wound healing is a highly dynamic and energy-requiring process, the role of metabolism remains largely unexplored. By combining transcriptomics and metabolomics of human skin biopsy samples, we mapped the core bioenergetic and metabolic changes in normal acute as well as chronic wounds in elderly subjects. We found upregulation of glycolysis, the tricarboxylic acid cycle, glutaminolysis, and β-oxidation in the later stages of acute wound healing and in chronic wounds. To ascertain the role of these metabolic pathways on wound healing, we targeted each pathway in a wound healing assay as well as in a human skin explant model using metabolic inhibitors and stimulants. Enhancement or inhibition of glycolysis and, to a lesser extent, glutaminolysis had a far greater impact on wound healing than similar manipulations of oxidative phosphorylation and fatty acid β-oxidation. These findings increase the understanding of wound metabolism and identify glycolysis and glutaminolysis as potential targets for therapeutic intervention.

2024-07-02 | MTBLS3315 | MetaboLights

Genome-wide plasma cell-free DNA methylation profiling in lung cancer patients using MeDIP-seq

Project description:As a non-invasive blood testing, the detection of cell-free DNA (cfDNA) methylation in plasma is raising increasing interest due to its diagnostic and biology applications. Although extensively used in cfDNA methylation analysis, bisulfite sequencing is less cost-effective. Through enriching methylated cfDNA fragments with MeDIP followed by deep sequencing, we aimed to characterize cfDNA methylome in cancer patients. In this study, we investigated the cfDNA methylation patterns in lung cancer patients by MeDIP-seq. MEDIPS package was used for the identification of differentially methylated regions (DMRs) between patients and normal ones. Overall, we identified 330 differentially methylated regions (DMRs) in gene promoter regions, 33 hypermethylation and 297 hypomethylation respectively, by comparing lung cancer patients and healthy individuals as controls. The 33 hypermethylation regions represent 32 genes. Some of the genes had been previously reported to be associated with lung cancers, such as GAS7, AQP10, HLF, CHRNA9 and HOPX. Taken together, our study provided an alternative method of cfDNA methylation analysis in lung cancer patients with potential clinical applications.

2019-03-31 | E-MTAB-7163 | biostudies-arrayexpress

Proteomic analysis of Caenorhabditis elegans wound model reveals novel molecular players involved in repair

Project description:Now a days, wound healing is becoming a global threat that impact economy of the country severely. Though the steps involved in wound healing are well characterised, direct therapeutics for the accelerated wound healing is comparatively less. This is solely because of the incomplete mechanism of healing and the lack of knowledge on molecular players involved in wound healing. Hence, in the present study, we have investigated the molecular players involved in wound healing process using a versatile model organism Caenorhabditis elegans through proteomic analyses. Especially, we have employed the high through put proteomic analyses tools such as 2-D GE and LCMS/MS analysis to uncover the molecular players involved in wound healing. As a result of 2-D GE analysis, a total of 35 differentially regulated proteins were identified during injury in which 22 and 13 proteins were upregulated and downregulated, respectively. Bioinformatics analyses result suggested that the upregulated proteins have crucial roles in serotonin/ acetyl choline synthesis and calcium signalling, whereas downregulated proteins were majorly involving in ubiquitin mediated proteolysis. Additionally, the mRNA levels of up and downregulated proteins were validated using qPCR analysis. Overall, the study suggested that injury initiates multiple molecular mechanisms to repair the damage.

2021-04-16 | PXD024629 | Pride

miRNA regulation in diabetes associated impaired wound healing

Project description:Circulating miRNAs constitute a novel class of disease biomarkers, which are altered in diabetes but the effect of diabetes associated inflammation as seen in chronic wounds is unknown. We here compared the miRNA pattern in diabetic patients in presence or absence of chronic wound with PAD. The clinical plasma samples were obtained from Heart and Diabetes centre, NRW and compared for plasma miRNA levels in 2 pools of 17 T2DM+PAD+Wound patients vs 2 pools from 20 T2DM controls

2015-06-09 | E-GEOD-49885 | biostudies-arrayexpress

Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (MethylCap-seq)

Project description:Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (MethylCap-seq)

| PRJNA736093 | ENA

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