The methylome and transcriptome of murine foetal skin and scarless wound healing
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ABSTRACT:
PROVIDER: PRJNA281101 | ENA |
REPOSITORIES: ENA
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Project description:Foetal skin is known to heal without scar. This ability is lost in the third trimester of gestation. In mouse, scarless wound healing was reported until the day 15-16 of gestation. A range of factors that could explain the mechanisms of scarless skin wound healing have been identified, to mention reduced immune response, a greater proportion of collagen type III, hyaluronic acid and transforming growth factor beta isoform 3. The involvement of epigenetic changes, which are known to determine developmental processes, has not been examined in the context of scarless foetal skin healing so far. We performed the microarray analysis methylome and transcriptome of murine foetal dorsal skin at embryonic day 15 contrasted with those in later phases at embryonic days 18-19 as well as the in the adult mouse. The group of genes which show decreased methylation status in the foetal skin before the loss of ability to scarless healing between embryonic day 15 and 18 are enriched with transcriptional factors involved in embryonic morphogenesis, epithelium development, neuron differentiation, and synapse functions. The genes with increased methylation after the transition are associated with cell death and epithelial cell differentiation, inflammatory and wounding response and the degradation of hyaluronic acid. A substantial part of DNA methylation differences observed between embryonic day 15 and 18 were retained later at embryonic day 19 and in adults and remarkably correlated with gene expression changes. A major part of genes encoding the key factors responsible for cutaneous wound healing show significant changes in gene expression following the transition from scar free to normal healing. The results show that skin methylome and transcriptome undergoe extensive alterations following the loss of ability to scarless healing, while the functions associated with the changes imply their central role in skin wound repair.
2016-12-31 | GSE67877 | GEO
Project description:Foetal skin is known to heal without scar. This ability is lost in the third trimester of gestation. In mouse, scarless wound healing was reported until the day 15-16 of gestation. A range of factors that could explain the mechanisms of scarless skin wound healing have been identified, to mention reduced immune response, a greater proportion of collagen type III, hyaluronic acid and transforming growth factor beta isoform 3. The involvement of epigenetic changes, which are known to determine developmental processes, has not been examined in the context of scarless foetal skin healing so far. We performed the microarray analysis methylome and transcriptome of murine foetal dorsal skin at embryonic day 15 contrasted with those in later phases at embryonic days 18-19 as well as the in the adult mouse. The group of genes which show decreased methylation status in the foetal skin before the loss of ability to scarless healing between embryonic day 15 and 18 are enriched with transcriptional factors involved in embryonic morphogenesis, epithelium development, neuron differentiation, and synapse functions. The genes with increased methylation after the transition are associated with cell death and epithelial cell differentiation, inflammatory and wounding response and the degradation of hyaluronic acid. A substantial part of DNA methylation differences observed between embryonic day 15 and 18 were retained later at embryonic day 19 and in adults and remarkably correlated with gene expression changes. A major part of genes encoding the key factors responsible for cutaneous wound healing show significant changes in gene expression following the transition from scar free to normal healing. The results show that skin methylome and transcriptome undergoe extensive alterations following the loss of ability to scarless healing, while the functions associated with the changes imply their central role in skin wound repair.
2016-12-31 | GSE67876 | GEO
Project description:The methylome of murine foetal skin and scarless wound healing
| PRJNA281103 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2016-12-31 | GSE67878 | GEO
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
Project description:The transcriptome of murine foetal skin and scarless wound healing
| PRJNA281102 | ENA
Project description:The process of wound healing in humans is poorly understood. To identify spatiotemporal gene expression patterns during human wound healing, we performed single cell and spatial transcriptomics profiling of human in vivo wound samples.
2024-09-04 | GSE241132 | GEO
Project description:Repairing a damaged body part is critical for the survival of an organism. Tissue damage induces rapid responses to activate downstream events including defense, regeneration and wound healing. Despite accumulating knowledge of early wound signaling including the orchestrated actions of phytohormones, electric circus and reactive oxygen species, our knowledge about the end point of a wound response - wound healing, is still limited. We observed that a local temperature reduction associated with the activation of cold-responsive genes occurred at wounding site on Arabidopsis leaves, which was likely caused by evaporative cooling. The disappearance of localized cooling and restoration of cold responsive genes to a steady state could be used as a quantitative readout of wound healing. Based on these observations, we developed a deep learning pipeline to monitor the dynamics of wound healing. We found that CBFs transcription factors relay injury-induced cooling signal to wound healing. Thus, our work provides a tool to quantify wound healing in plants and advances our understanding of tissue repair in plants.
2025-06-25 | GSE293328 | GEO
Project description:S.ciliatum wound healing - transcriptome sequencing
| PRJEB49227 | ENA