Exploring mechanisms of scar-free skin wound healing in adult zebrafish
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ABSTRACT:
PROVIDER: PRJNA1310598 | ENA |
REPOSITORIES: ENA
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Project description:We performed single-cell RNA sequencing to better characterize the dynamics and heterogeneity of involved cell types during different stages of zebrafish cutaneous wound healing.
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Project description:Salamanders, such as the Mexican axolotl, are some of the few vertebrates fortunate in their ability to regenerate diverse structures after injury. Unlike mammals they are able to regenerate a fully functional spinal cord after injury. Throughout human life, many cells and certain tissues, such as hair follicle stem cells and liver, can be continuously replaced to maintain functional integrity in response to normal daily wear and tear. However, the human response to more serious tissue damage is limited to relatively primitive wound healing, whereby collagenous scar tissue fills the injury site, assuring the tissue’s structural integrity but often resulting in a debilitating loss of functionality. In contrast many vertebrates, including axolotls, have remarkable regenerative capacity including the functional regeneration of full thickness wounds. Here, we have identified a novel role for SALL4 in regulating collagen transcriptional after injury that is essential to ensure perfect skin regeneration in axolotl.
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2010-07-20 | E-GEOD-23006 | biostudies-arrayexpress
Project description:Effectively managing skin wounds to achieve quick and scarless healing is a significant clinical challenge. Several cell types participate in wound healing, including keratinocytes, fibroblasts, and many others. Human adipose-derived mesenchymal stem cell-derived exosomes (hADSC-Exos) are regarded as promising therapeutic choice. However, a comprehensive understanding of what mechanisms promote regenerative healing respond to hADSC-Exos treatment is still limited. Here, we utilize a high-resolution single-cell RNA sequencing analysis (scRNA-seq) from adult wild-type mice, postoperative day (POD) 14 mice and hADSC-Exos-treated postoperative day (POD) 14 mice. hADSC-Exos influences epithelial cells and fibroblasts, leading to scar-free wound healing. Among epithelial cell subtypes, Lef1high proliferating keratinocytes (prolif KC) are particularly remodeled by hADSC-Exos. Prolif KC exhibit epithelial-mesenchymal plasticity (EMP). The cell-cell communication between keratinocytes and fibroblasts in anti-scar healing is modulated by TGF-β1, which promote EMP transition cascade. hADSC-Exos may inhibit wound fibrosis through the 14-3-3Zeta-YES-associated protein (YAP)-hippo signaling pathway. This study enhances our understanding of epithelial cell diversity and interactions in wound healing, highlighting hADSC-Exos-induced prolif KC as potential reprogramming targets. These epithelial cells present promising therapeutic targets for improving wound healing strategies.
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Project description:Mammalian skin wounds typically heal with a scar, characterized by fibrotic tissue that disrupts original tissue architecture and function. Therapies to reduce fibrosis and scar formation remain a large unmet clinical need. Rosemary extract, particularly in the form of topical oils and creams, has gained massive popularity within the general public as a potential treatment to reduce scar formation. However, its efficacy and potential mechanism of action remain unknown. We show in adult wound healing mouse models that an ethanol-based rosemary extract reduces fibrosis and promotes scarless wound healing. More specifically, carnosic acid within rosemary leaves acts as an active ingredient and stimulates the TRPA1 nociceptor on cutaneous sensory neurons to promote scarless wound healing. Mice lacking TRPA1 on sensory neurons do not exhibit rosemary-induced tissue regeneration. Taken together, topical rosemary extract may be an effective and cost-efficient therapeutic to reduce scar formation in skin wounds.
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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.
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Project description:By utilizing single-cell analysis at different times after P2 injury(0, 3, and 5 dpi), we discovered that neonatal microglia undergo a transient activation and play at least two critical roles in scar-free healing. First, they transiently secrete fibronectin and its binding proteins, to form extracellular matrix bridges that ligate the severed ends. Second, neonatal, but not adult, microglia express a number of extracellular and intracellular peptidase inhibitors, along with other molecules involved in inflammatory resolution.
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