MiR-Seq on paired skin and oral mucosal wound healing
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE121996 | GEO | 2019/05/29
REPOSITORIES: GEO
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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.
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Project description:miR-Seq on paired skin and oral mucosal wound healing
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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.
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Project description:Rapid and scarless wound repair is a hallmark of the oral mucosa, yet the cellular and molecular mechanisms that enable this regeneration remain unclear. By comparing populations of oral mucosal fibroblasts (OMFs) and facial skin fibroblasts (FSFs), we have identified the mechanisms that facilitate regeneration over fibrosis. We found that OMFs utilize Growth arrest specific-6 (GAS6)-AXL signaling to suppress fibrosis-related mechanosignaling via Focal adhesion kinase (FAK). Inhibition and knockdown of AXL in the oral mucosa resulted in fibrotic wounds and increased activation of FAK. At the same time, stimulation of AXL in the facial skin yielded wounds that heal regeneratively. Rare human oral scars that resulted from repetitive injury showed decreased expression of GAS6/AXL and increased FAK. Activating AXL in repetitively injured mouse oral tissue resulted in better wound healing outcomes and reduced scarring. Together, our work demonstrates that AXL signaling is necessary for regenerative wound healing in the oral mucosa and sufficient to limit facial skin fibrosis.
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Project description:Rapid and scarless wound repair is a hallmark of the oral mucosa, yet the cellular and molecular mechanisms that enable this regeneration remain unclear. By comparing populations of oral mucosal fibroblasts (OMFs) and facial skin fibroblasts (FSFs), we have identified the mechanisms that facilitate regeneration over fibrosis. We found that OMFs utilize Growth arrest specific-6 (GAS6)-AXL signaling to suppress fibrosis-related mechanosignaling via Focal adhesion kinase (FAK). Inhibition and knockdown of AXL in the oral mucosa resulted in fibrotic wounds and increased activation of FAK. At the same time, stimulation of AXL in the facial skin yielded wounds that heal regeneratively. Rare human oral scars that resulted from repetitive injury showed decreased expression of GAS6/AXL and increased FAK. Activating AXL in repetitively injured mouse oral tissue resulted in better wound healing outcomes and reduced scarring. Together, our work demonstrates that AXL signaling is necessary for regenerative wound healing in the oral mucosa and sufficient to limit facial skin fibrosis.
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Project description:Rapid and scarless wound repair is a hallmark of the oral mucosa, yet the cellular and molecular mechanisms that enable this regeneration remain unclear. By comparing populations of oral mucosal fibroblasts (OMFs) and facial skin fibroblasts (FSFs), we have identified the mechanisms that facilitate regeneration over fibrosis. We found that OMFs utilize Growth arrest specific-6 (GAS6)-AXL signaling to suppress fibrosis-related mechanosignaling via Focal adhesion kinase (FAK). Inhibition and knockdown of AXL in the oral mucosa resulted in fibrotic wounds and increased activation of FAK. At the same time, stimulation of AXL in the facial skin yielded wounds that heal regeneratively. Rare human oral scars that resulted from repetitive injury showed decreased expression of GAS6/AXL and increased FAK. Activating AXL in repetitively injured mouse oral tissue resulted in better wound healing outcomes and reduced scarring. Together, our work demonstrates that AXL signaling is necessary for regenerative wound healing in the oral mucosa and sufficient to limit facial skin fibrosis.
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Project description:Rapid and scarless wound repair is a hallmark of the oral mucosa, yet the cellular and molecular mechanisms that enable this regeneration remain unclear. By comparing populations of oral mucosal fibroblasts (OMFs) and facial skin fibroblasts (FSFs), we have identified the mechanisms that facilitate regeneration over fibrosis. We found that OMFs utilize Growth arrest specific-6 (GAS6)-AXL signaling to suppress fibrosis-related mechanosignaling via Focal adhesion kinase (FAK). Inhibition and knockdown of AXL in the oral mucosa resulted in fibrotic wounds and increased activation of FAK. At the same time, stimulation of AXL in the facial skin yielded wounds that heal regeneratively. Rare human oral scars that resulted from repetitive injury showed decreased expression of GAS6/AXL and increased FAK. Activating AXL in repetitively injured mouse oral tissue resulted in better wound healing outcomes and reduced scarring. Together, our work demonstrates that AXL signaling is necessary for regenerative wound healing in the oral mucosa and sufficient to limit facial skin fibrosis.
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Project description:Wound healing within the oral mucosa results in minimal scar formation compared to wounds within the skin. We have recently demonstrated distinct differences in the ageing profiles of cells (oral mucosal and patient-matched skin fibroblasts) isolated from these tissues. We hypothesize that the increased replicative potential of oral mucosal fibroblasts may confer upon them preferential wound healing capacities. Passage-matched early cultures of oral mucosal fibroblasts and skin fibroblasts demonstrated distinct gene expression profiles with a number of genes linked to wound healing/tissue repair. We analyzed the gene expression profiles of oral mucosal and patient-matched skin fibroblasts for multiple patients both prior to (0h) and (6h) following a wounding stimulus.
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