Gene expression at skin wound sites of WT and FoxO1+/- mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE48473 | GEO | 2014/06/01
SECONDARY ACCESSION(S): PRJNA210259
REPOSITORIES: GEO
Similar Datasets
Project description:In order to determine molecular mechanisms of faster skin wound healing under decreasing FoxO1 protein expression, we performed microarray analysis on 3 days skin wounded samples from FoxO1+/- and WT mice. Skin wound-induced gene expression in WT and FoxO1+/- mice were measured on 3 days after injury. Three independent experiments were performed at each mouse.
2014-06-01 | E-GEOD-48473 | biostudies-arrayexpress
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:Defective fibroblast migration cause delayed wound healing (WH) and chronic skin lesions. Autologous micrograft (AMG) therapies have recently emerged as a new effective treatment able to improve wound healing capacity. However, the molecular mechanisms connecting their beneficial outcomes with the wound healing process are still unrevealed. Here, we show that AMG modulates primary fibroblast migration and accelerates skin re-epithelialization without affecting cell proliferation. We demonstrate that AMG is enriched in a pool of WH-associated growth factors that may provide the initiation signal for faster endogenous wound healing response. This, in turn leads to increased cell migration rate by elevating activity of ERK and subsequent activation of matrix metalloproteinase expression and their extracellular enzymatic activity. Moreover, AMG-treated wounds showed increased granulation tissue formation and organized collagen content. Overall, we shed light on AMG molecular mechanism supporting its potential to trigger highly improved wound healing process.
2020-01-01 | GSE123829 | GEO
Project description:To investigate how HOXA3 expression in wound tissue alters gene expression to control selective recruitment of bone marrow-derived cell populations, we utilized murine whole genome expression arrays (MEEBO arrays) to identify differentially expressed genes in cutaneous wounds from db/db (diabetic) mice treated with either CMV-HOXA3 or control plasmid. In addition to unwounded control skin, we chose day 4 as the time point to harvest the wounds for RNA isolation, which represents the transition from inflammatory to proliferative phase of wound repair, and precedes the observed differences in BMDC mobilization and recruitment at day 7. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Disease State: cutaneous wound/control skin unwounded skin, wounded skin treated with control plasmid, wounded skin treated with HOXA3
2009-10-12 | E-GEOD-13324 | biostudies-arrayexpress
Project description:Diabetic foot ulcers (DFU) are one of the major complications in type II diabetes patients and can result in amputation and morbidity. Although multiple approaches are used clinically to help wound closure, many patients still lack adequate treatment. Here we show that IL-20 subfamily cytokines are upregulated during normal wound healing. While there is a redundant role for each individual cytokine in this subfamily in wound healing, mice deficient in IL-22R, the common receptor chain for IL-20, IL-22, and IL-24, display a significant delay in wound healing. Furthermore, IL-20, IL-22 and IL-24 are all able to promote wound healing in type II diabetic db/db mice. When compared to other growth factors such as VEGF and PDGF that accelerate wound healing in this model, IL-22 uniquely induced genes involved in reepithelialization, tissue remodeling and innate host defense mechanisms from wounded skin. Interestingly, IL-22 treatment showed superior efficacy compared to PDGF or VEGF in an infectious diabetic wound model. Taken together, our data suggest that IL-20 subfamily cytokines, particularly IL-20, IL-22, and IL-24, might provide therapeutic benefit for patients with DFU.
2017-03-08 | GSE80419 | GEO
Project description:Studying the transcriptomic response of different epidermal stem cell populations to wounding has been difficult due to intermixing of wound healing and homeostastic cells from different stem cell pools in bulk-cell sequencing setups. Here, we circumvent those problems by using a single-cell sequencing approach. We randomly sequenced the traced progeny of either Lgr5 or Lgr6 stem cells isolated from wounded or unwounded skin 0 day (control), 1 d, 4 d, 7 d, 10 d or more than 1 month after wounding. We then identified Lgr5 or Lgr6 wound cells using a computational approach. Wound cells were defined by using a negative binominal Naïve Bayes classifier with 0-day control cells (unwounded mice) as reference. Wound cell populations were defined by clustering wound cells in t-SNE space using k-means clustering.
2018-04-01 | E-MTAB-6583 | biostudies-arrayexpress
Project description:Human in vivo skin wound: Non-wounded skin was obtained by taking punch biopsies from three healthy donors (donor 1,2 and 3). The samples were termed 'skin day 0 in vivo wound'. Skin wound samples were retrieved by making new punch biopsies from the edge of the original biopsies after four days. These samples were termed 'skin day 4 in vivo wound'. As much dermal tissue as possible was removed by dissection to make sure mainly epidermis was present in the samples. The samples were washed in NaCl to possible remove infiltrating inflammatory cells before RNA isolation. Ex vivo skin wounds: Skin was obtained from three healthy donors following reduction surgery (donor 1, 2, and 3). As much dermal tissue as possible was removed dissection. These samples were termed 'skin day 0 ex vivo wound'. Skin was sliced into 1x10 mm slices and incubated in keratinocyte medium for four days with either 1:1000 fold dilution of DMSO or 10 micromolar AG-1478 (dissolved in DMSO). Again as much dermal tissue was removed by dissection as possible before RNA was isolated. These samples were termed 'skin day 4 ex vivo wound' and 'skin day 4 AG-1478 ex vivo wound'. By comparing the gene expression day 4 in ex vivo wound with in vivo wounds it was possible to see which part of the gene expression in wounded skin that was due to the epidermal reaction to injury and how much was due to stimuli from infiltrating inflammatory cells absent in the ex vivo skin wounds. By comparing the data from ex vivo skin wounds day 4 with and without the EGFR-inhibitor AG-1478, it was possible to look at the importance of the EGF-receptor of EGFR for the gene expression in ex vivo wounded skin.
2011-09-13 | E-MEXP-3305 | biostudies-arrayexpress
Project description:Now a days, wound healing is becoming a global threat that impact economy of the country severely. Though the steps involved in wound healing are well characterised, direct therapeutics for the accelerated wound healing is comparatively less. This is solely because of the incomplete mechanism of healing and the lack of knowledge on molecular players involved in wound healing. Hence, in the present study, we have investigated the molecular players involved in wound healing process using a versatile model organism Caenorhabditis elegans through proteomic analyses. Especially, we have employed the high through put proteomic analyses tools such as 2-D GE and LCMS/MS analysis to uncover the molecular players involved in wound healing. As a result of LC-MS/MS analysis at 0 and 24 h, a total of 435 proteins were regulated in both unwounded and wounded conditions in which 13 and 10 proteins were significantly differential regulated. Bioinformatics analyses result suggested that molecular players involved in cortical actin cytoskeleton organization, protein phosphatase binding, and proton transporting ATP synthase activity were identified at 0 h; skeletal muscle myosin thick filament assembly, actin filament depolymerization were identified at 24 h.
2021-04-16 | PXD024744 | Pride
Project description:The cornea is a transparent organ, highly specialized and unique that is continually subjected to abrasive forces and occasional mechanical or chemical trauma because of its anatomical localization. Upon injury, the extracellular matrix (ECM) rapidly changes to promote wound healing through integrin-dependent activation of specific signal transduction mediators whose contribution is to favor faster closure of the wound by altering the adhesive and migratory properties of the cells surrounding the damaged area. In this study, we exploited the human tissue-engineered cornea (hTECs) as a model to study the signal transduction pathways that participate to corneal wound healing. By exploiting both gene profiling and activated kinases arrays, we could demonstrate the occurrence of important alterations in the level of expression and activation of a few mediators from the PI3K/Akt and CREB pathways in response to the ECM remodeling taking place during wound healing of damaged hTECs. Pharmacological inhibition of CREB with C646 considerably accelerated wound closure compared to controls. This process was considerably accelerated further when both C646 and SC79, an Akt agonist, were added together to wounded hTECs. Therefore, our study demonstrate that proper corneal wound healing requires the activation of Akt together with the inhibition of CREB and that wound healing in vitro can be altered by the use of pharmacological inhibitors (such as C646) or agonists (such as SC79) of these mediators.
2018-04-21 | GSE113438 | GEO
Project description:Mice were wounded and skin samples of the scar collected on the day of wound closure. We compared Mixed mice (B6/FVB/SJL), a strain of high regeneration, versus C57bl mice, a strain of low regeneration. Whole skin biopsies of wound scars were submitted for Affymetrix Exon arrays. 4 mice each of 2 distinct strains of differing regeneration levels were collected.
2015-08-05 | E-GEOD-50418 | biostudies-arrayexpress