Spatiotemporal Single-Cell Roadmap of Human Skin Wound Healing (Spatial)
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PROVIDER: PRJNA1006428 | ENA |
REPOSITORIES: ENA
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Project description:The process of wound healing in humans is poorly understood. To identify spatiotemporal gene expression patterns during human wound healing, we performed spatial transcriptomics profiling of human in vivo wound samples.
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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.
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Project description:Spatiotemporal Single-Cell Roadmap of Human Skin Wound Healing (Single-cell-Wound)
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Project description:Spatiotemporal Single-Cell Roadmap of Human Skin Wound Healing (Single-cell-VU)
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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:In order to clarify the human response of re-epithelialization, we biopsied split-thickness skin graft donor site wounds immediately before and after harvesting, as well as during the healing process 3 and 7 days thereafter. Altogether 25 biopsies from 8 patients qualified for the study. All samples were analysed by genome-wide microarrays. Here we identified the genes associated with normal skin re-epithelialization on time-scale, and organized them by similarities according to their induction or suppression patterns during wound healing. Overall 25 samples were analyzed
2011-04-29 | E-GEOD-28914 | biostudies-arrayexpress
Project description:Diabetic foot ulcer (DFU) is a serious complication of diabetes mellitus, which causes great health damage and economic burden to patients. The pathogenesis of DFU is not fully understood.We screened wound healing-related genes using bioinformatics analysis, and full-thickness skin injury mice model and cellular assays were used to explore the role of target genes in diabetic wound healing. SFRP2 was identified as a wound healing-related gene, and the expression of SFRP2 is associated with immune cell infiltration in DFU. In vivo study showed that suppression of SFRP2 delayed the wound healing process of diabetic mice, impeded angiogenesis and matrix remodeling, and increased macrophage infiltration in wound tissues. In addition, suppression of SFRP2 enhanced M1 polarization in both the early and later stage of wound healing, and decreased M2 polarization in the later stage, which impeded the transition of M1 to M2 polarization of wound healing. Moreover, suppression of SFRP2 affected the transcriptome signatures-related to inflammatory response and energy metabolism at the early stage of wound healing. Extracellular flux analysis (EFA) showed that suppression of SFRP2 decreased mitochondrial energy metabolism and increased glycolysis in injury-related macrophages. Furthermore, suppression of SFRP2 inhibited transcriptome signaturesrelated to carbohydrate metabolism, lipid metabolism and amino acid metabolism, which consists the three main components of energy metabolism of macrophages. In conclusions, SFRP2 may function as a wound healing-related gene in DFU, and suppression of SFRP2 impaired diabetic wound healing by compromising the M1-to-M2 transition of macrophages and modulating the balance between mitochondrial energy metabolism and glycolysis.
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Project description:When compared to skin, oral mucosal wounds heal rapidly and with reduced scar formation. This study used an Affymetrix microarray platform to compare the transcriptomes of oral mucosa and skin wounds in order to identify critical differences in the healing response at these two sites. Using microarrays, we explored the differences in gene expression in skin and oral mucosal wound healing in a murine model of paired equivalent-sized wounds. Samples were examined from day 0 to day 10 and spanned all stages of the wound healing process. Unwounded matched tissue was used as a control. Tissue samples collected at each post-wounding time point, as well as control samples, were represented by 3 biological replicates.
2010-07-20 | E-GEOD-23006 | biostudies-arrayexpress
Project description:Wound healing is essential to repair the skin after injury. In the epidermis, distinct stem cells (SCs) populations contribute to wound healing. However, how SCs balance proliferation, differentiation and migration to repair a wound remains poorly understood. Here we show the cellular and molecular mechanisms that regulate wound healing in mouse tail epidermis. Using a combination of proliferation kinetics experiments and molecular profiling, we identify the gene signatures associated with proliferation, differentiation and migration in different regions surrounding the wound. Functional experiments show that SC proliferation, migration and differentiation can be uncoupled during wound healing. Lineage tracing and quantitative clonal analysis reveal that, following wounding, progenitors divide more rapidly, but conserve their homeostatic mode of division, leading to their rapid depletion whereas SCs become active, giving rise to new progenitors that expand and repair the wound. These results have important implications for tissue regeneration, acute and chronic wound disorders.
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