Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA129913 | ENA |
REPOSITORIES: ENA
Similar Datasets
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 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.
2011-01-01 | GSE21648 | GEO
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. Differences in the gene expression profiles of oral mucosal and patient-matched skin fibroblasts were anlazyed for multiple patients both prior to (0h) and (6h) following a wounding stimulus. Serum starvation and subsequent stimulation provides a model for wounding and RNA extracted at 0h and 6h following this stimulus was hybridized to Affymetrix microarrays for analysis. We sought to compare the expression profiles both between oral and normal fibroblasts, in both serum depleted and stimulated conditions and also compare differences between patients.
2011-01-01 | E-GEOD-21648 | biostudies-arrayexpress
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.
2025-04-30 | GSE287947 | GEO
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.
2025-04-30 | GSE287528 | GEO
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.
2025-04-30 | GSE287384 | GEO
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.
2025-04-30 | GSE287839 | GEO
Project description:To delineate the role of microRNAs in the site-specific injury response, we compared the microRNAome of skin and oral mucosa both at baseline and throughout the time course of wound healing.
2019-05-29 | GSE121996 | GEO
Project description:Compare with facial skin, oral mucosa has a high regenerative capacity and rapid healing efficiency, which has long been recognized as an ideal system of wound resolution. To decipher the underlying molecular mechanisms fostering this optimal healing process, we created a parallel injury model for both the oral and facial skin within the same mice. Utilizing single-cell transcriptomics (scRNA-seq) analysis, we were able to illuminate the diverse cell populations and the intricate cell-to-cell interactions taking place at a single cell level. Leveraging tools such as CytoTRACE, along with cell trajectory and RNA velocity analyses, we pinpointed fibroblast progenitors. Through the employment of GSEA and CellChat analyses, corroborated by flow cytometry and immunofluorescence staining, we demonstrated that IL-1β derived from macrophages augments oxidative phosphorylation in Il1rl1+ progenitors in skin. This points to a rapid response mechanism facilitated by heightened cell-cell interactions through IL-1β signals. We elucidated that the underlying mechanism involves a metabolic reprogramming in oral Il1rl1+ fibroblast progenitors driven by IL-1β/IL1R1, triggering the activation of the NFκB signaling pathway. This shift transitions the metabolic state from glycolysis to oxidative phosphorylation, favoring stem cell differentiation over proliferation and consequently accelerating wound healing in the oral mucosa.
2025-09-03 | GSE256125 | GEO
Project description:Fibroblasts are abundant structural cells that produce extracellular matrix components and are essential for tissue repair following an injury. Emerging evidence highlights a crucial immunomodulatory role of fibroblasts in health and disease, which is incompletely explored in the wound healing field. Here, we used an oral wound healing model that heals exceptionally fast with minimal scarring and investigated if select fibroblasts are endowed with immune-regulatory functions that can have an impact on optimal healing outcomes. We identified PI16+ oral reticular fibroblasts to be highly enriched in interleukin-33 (IL33), an alarmin cytokine that is rapidly released during the early stages of wound healing. Using mice with lineage-specific, inducible deletion of IL33, we found that baseline expression of IL33 from fibroblasts but not keratinocytes was necessary for proper wound healing in oral mucosa. Singe cell RNA-sequencing (scRNA-seq)analysis revealed that regulatory T cells (Tregs) respond to IL33 and upregulate the expression of a pro-inflammatory cytokine MIF and an anti-inflammatory cytokine TGFB1, which was validated in vivo. Mechanistically, MIF promotes recruitment of angiogenic monocytes to facilitate blood vessel formation in healing wounds, whereas TGFB1 supports an early transition of macrophages to a pro-resolving phenotype. Importantly, we show that human oral mucosa, but not skin, harbors IL33+ PI16+ reticular fibroblasts in deeper aspects of the connective tissue and that Tregs express MIF and TGFB1 in regenerating oral mucosa. Together, our study unveils an essential role of IL33+ oral reticular fibroblasts for the modulation of acute inflammation by engaging Tregs that promote angiogenesis and resolution of inflammation in wound healing.
2026-01-08 | GSE292645 | GEO