Mus musculus
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ABSTRACT:
PROVIDER: PRJNA231921 | ENA |
REPOSITORIES: ENA
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Project description:Skin wound healing is one of the major prevalent medical problems in the worldwide. Wound healing involves multi-process synergy and re-epithelialization is an essential part of wound healing. Histone H3K36 tri-methylase Setd2 has been extensively studied in different biological processes and diseases. However, the function of Setd2 in the wound healing remains unclear. To elucidate the biological role of Setd2 in the skin wound healing, conditional gene targeting was employed to establish epidermis-specific Setd2-deficient mice. We found that Setd2 deficiency resulted in accelerated re-epithelialization during cutaneous wound healing by promoting keratinocytes proliferation and migration. Furthermore, we demonstrated that loss of Setd2 activated the AKT/mTOR pathway, and pharmacological inhibitions of AKT and mTOR with MK2206 and rapamycin delayed wound closure, respectively. In conclusion, our results reveal the essential role of Setd2 in skin wound healing that is Setd2 loss promotes cutaneous wound healing via activation of AKT/mTOR signaling.
2020-12-25 | GSE163860 | GEO
Project description:Skin wound healing is one of the major prevalent medical problems in the worldwide. Wound healing involves multi-process synergy and re-epithelialization is an essential part of wound healing. Histone H3K36 tri-methylase Setd2 has been extensively studied in different biological processes and diseases. However, the function of Setd2 in the wound healing remains unclear. To elucidate the biological role of Setd2 in the skin wound healing, conditional gene targeting was employed to establish epidermis-specific Setd2-deficient mice. We found that Setd2 deficiency resulted in accelerated re-epithelialization during cutaneous wound healing by promoting keratinocytes proliferation and migration. Furthermore, we demonstrated that loss of Setd2 activated the AKT/mTOR pathway, and pharmacological inhibitions of AKT and mTOR with MK2206 and rapamycin delayed wound closure, respectively. In conclusion, our results reveal the essential role of Setd2 in skin wound healing that is Setd2 loss promotes cutaneous wound healing via activation of AKT/mTOR signaling.
2020-12-25 | GSE163858 | GEO
Project description:Objective: Ionizing radiation (IR) therapy, commonly used in cancer treatment, has detrimental effects on the skin. When combined with surgical resection, IR leads to persistent wounds and forms a significant side effect, making wound healing difficult. This study aimed to understand the mechanisms underlying IR-induced wound damage and develop treatment methods. Approach: A mouse model of IR was created by exposing mice to 7Gy of radiation after skin excision. The temporal changes of epidermal stem cells (EPSCs) and wound healing were examined. RNA-seq analysis was performed on skin tissues to investigate regulatory mechanisms during the healing process. Topical application of TGFβ was used to assess its impact on wound healing. Results: Mice in the IR group exhibited prolonged wound healing time, and the healing rate was significantly reduced. IR exposure decreased Ki67+/K14+ cells (proliferating EPSCs), reduced the expression levels of K14 and K15. The RNA-seq results revealed a significant decrease in epidermal stem cell-related genes following IR. Additionally, the TGFβ-SMAD pathway exhibited temporal changes during the wound healing process, while pre-treatment with TGFβ1 significantly promotes the healing of IR-induced wounds. Innovation: TGF-β1 activated the TGFβ-SMAD pathway and promotes wound healing after ionizing radiation. Conclusions: These findings indicate that IR diminishes the population of epidermal stem cells (EPSCs), thereby impeding the healing process by disrupting the TGFβ-Smad pathway. However, the external application of TGFβ1 to the wound area effectively improves IR-induced skin damage and exhibits promising therapeutic effects. These findings provide intervention targets and agents for the clinical applications.
2025-08-15 | GSE241297 | GEO
Project description:Standardized skin wounds were established surgically on mice and allowed to heal during a 15-day period. Expression of genes related to heparan sulfate biosynthesis was studied in wound bed and edges during the healing process. Total RNA was isolated from wound edge (regenerating skin) and wound bed at 2, 6 and 15 days post wounding, as well as from intact control skin. Three animals were used for each time point.
2010-05-22 | E-GEOD-7435 | biostudies-arrayexpress
Project description:Wound healing is one fundamental physiological process which maintains the integrity of skin through a series of well-orchestrated biological and molecular events,effective resolution of inflammation is crucial for wound healing We used microarrays to characterize molecular mechanisms of wound healing with Spink7 KO mice of up-regulated genes during this process.
2025-04-02 | GSE282599 | 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:Changes in miRNA expression during wound healing in mouse aged skin
| PRJNA380435 | ENA
Project description:An effective healing response is critical to healthy aging. Thus, the connection of regeneration and aging is needed to understand the complicated age-related healing process. Energy metabolism has been a common hallmark of both studies. In recent years, it become an emerging factor of skin homeostasis. Adenine nucleotide translocase-2 (ANT2) is a known cell proliferation marker and mediator of ATP import into mitochondria for energy homeostasis. Although energy homeostasis and the maintenance of mitochondrial function are critical for wound healing, the role of ANT2 in wound healing has not been elucidated. We found that ANT2 expression decreased during aging in mouse skin as well as during cellular senescence. Interestingly, overexpression of ANT2 in aged mouse skin promoted the healing of full-thickness cutaneous wounds. In addition, upregulation of ANT2 in replicative senescent human diploid dermal fibroblasts (HDFs) induced cell proliferation and migration, which are critical for the wound healing process. Furthermore, overexpression of ANT2 increased ATP production rate by activating the glycolysis pathway and also increased mitophagy, both of which are involved in energy homeostasis. Notably, ANT2-mediated upregulation of HSPA6 in aged HDFs inhibited the expression of pro-inflammatory genes that mediate cellular senescence and mitochondrial damage. This study demonstrates a new physiological role of ANT2 in skin wound healing via regulation of cell proliferation, energy homeostasis, and inflammation. Thus, our study links energy metabolism to skin homeostasis and identifies a genetic factor for improving wound healing with aging model.
2022-11-21 | GSE206141 | GEO
Project description:To develop effective therapeutic interventions that prevent scar formation and encourage regeneration of healthy skin, we need to better understand the cellular and molecular process that are engaged during the wound healing process in humans. However, our cellular and molecular understanding of how humans heal deep dermal wounds remains limited. Our recent work using different animal models of skin wound healing has identified the acute wound healing immune response as a key determinant of terminal fibrotic outcomes. Here, our goal is to compare the immune response during human wound healing to datasets we have generated from large animal models that are capable of scarless healing, in order to determine how to most appropriately modify the process in humans to improve outcomes (and mitigate scar).
2026-05-01 | GSE254329 | GEO
Project description:Background The skin maintains the body’s integrity and serves as the first line of defence against pathogens, stressors and mechanical injuries. Despite the global significance of salmon in aquaculture, how cells transcriptomic profile varies during wound healing, remains unexplored. Teleost contain adult pluripotent cells that differentiate into various tissues, including bone, cartilage, tendon, ligament, adipose, dermis, muscle and connective tissue within the skin. These cells are pivotal for preserving the integrity of skin tissue throughout an organism´s lifespan and actively participate in the wound healing processes. In this study, we characterise the transcriptomic profiles of putative mesenchymal stromal cells (fibroblast-like adult stem cells) in healthy Atlantic salmon tissue and during the wound healing process. Results Single-nucleus sequencing and spatial transcriptomics were used to detect transcriptomic changes occurring during wound healing that are commonly associated with mesenchymal stromal cells. We followed the transcriptomic activity of these cells during an in vivo wound healing time course study showing that these cells become more transcriptionally active during the remodelling stage of wound healing. The changes detected give insights into the potential differentiation pathways leading to osteogenic and fibroblast lineages in the skin of Atlantic salmon. Conclusions We chart the transcriptomic activity of sub-clusters of putative differentiating stromal cells during the process of wound healing for the first time, revealing different spatial niches of the various putative MSC subclusters, and setting the stage for further investigation of the manipulation of transitioning cell types to improve fish health. KEYWORDS: Salmo salar, skin, mesenchymal stromal cells, single-cell sequencing, spatial transcriptomics, wound healing, spatial niche.
2025-01-15 | GSE287051 | GEO