Changes in transcriptome during excisional cutaneous murine wound healing
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE76144 | GEO | 2015/12/19
SECONDARY ACCESSION(S): PRJNA306422
REPOSITORIES: GEO
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Project description:Using microarray analysis, we explored the differences in gene expression in wounded and intact skin using murine model. Injured skin samples were examined at days 1 and 4 post injury. The results provide the detailed molecular profile of the the genetic response to injury. Two full-thickness dermal wounds were made on the opposite sides of the midline of each mouse using a 4 mm punch biopsy instrument. Wounds were made through the epidermis, dermis, and subcutaneous tissue layers while leaving the fascia intact. At a specified time point after the wounding (1 and 4 days), mice were sacrificed by carbon dioxide inhalation. The wounds and surrounding tissues or intact skin samples were removed with an 8 mm biopsy punch.
2015-12-19 | E-GEOD-76144 | 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: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:Adaptive cellular reprogramming is an emerging field to study promotion of a host’s intrinsic healing strategies through changing one somatic cell type into another state or fate; tissue injury is known to enhance such cell conversions. Here we identify a molecular pathway in injured skin, whereby a subset of dermal fibroblasts displays a novel vasculogenic state change with gain in vasculogenic transcripts and endothelial cell-like functions without losing core fibroblast lineage fate phenotypic, functional, and transcriptional characteristics. Removal of microRNA suppression of FLI1 transcription in fibroblasts results in upregulation of a cascade of vasculogenic molecules that heralds the vasculogenic state change in some fibroblasts. FLI1 dependent vasculogenic fibroblast subset emergence in injured skin is blunted in poorly healing skin wounds of diabetic animals but can be restored through topical tissue nanotransfection of a single anti-microRNA oligonucleotide, to rescue tissue perfusion and wound healing. Augmenting a physiologic tissue injury adaptive response mechanism that produces vasculogenic fibroblasts opens new avenues for therapeutic tissue vascularization of ischemic conditions.
2022-12-27 | GSE167406 | GEO
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:The interaction between neurogenesis and angiogenesis after traumatic brain injury is a complex and dynamic process. To resolve this, we chose the zebrafish model organism for studying brain wound healing via systems biology approach. Transcriptome microarray data and histological analysis of injured fish were sampled at different time points during recovery process. Time-course microarray data following wound healing of zebrafish were obtained. From this set of data, we constructed two intracellular proteinM-bM-^@M-^Sprotein interaction (PPI) networks for the traumatic brain injury healing mechanism. Each fish in each group was injured by a 1.5 mm, 27G needle tip from day 0 to 28, respectively. These injured fish were collected at 0, 0.25, 1, 3, 6, 10, 15, 21, 28 dpi (day post injury). 0.625M-NM-<g of Cy3 cRNA for C. albicans array and 1.65 M-NM-<g of Cy3 cRNA for zebrafish array was fragmented to an average size of about 50-100 nucleotides by incubation with fragmentation buffer at 60M-BM-0C for 30 minutes. Each time point contain two biological repeats.
2014-09-30 | E-GEOD-56375 | biostudies-arrayexpress
Project description:Transcription profiling by array of wounded Nematostella juvenile polyps compared against uninjured animals and animals exposed to the MAPK inhibitor U0126
2014-03-10 | E-MTAB-2341 | biostudies-arrayexpress
Project description:The vitamin D receptor (VDR) regulates cell proliferation and differentiation including epidermal keratinocytes by modulating transcription of its target genes. We are investigating the role of VDR in epidermal stem cells and their progenies in the regeneration process of epidermis and hair in the skin. VDR null mice are utilized in which VDR is specifically deleted in keratin 14 (K14) expressing keratinocytes by Cre-lox strategy. The impact of VDR deletion was evaluated by comparison of VDR null mice with no cre littermate control mice. The VDR was abundantly expressed in potential epidermal stem cells including basal cells in interfollicular epidermis (IFE), and in CD34 expressing bulge keratinocytes in hair follicles. Gene expression profiles and subsequent pathway analysis of stem cell enriched keratinocyte populations revealed that the VDR deletion significantly suppressed β-catenin signaling as well as VDR signaling. The role of VDR in epidermal stem cells was studied during hair follicle cycling and wound healing processes. The epidermal stem cells were not appropriately stimulated by hair depilation, and did not reinitiate anagen in the hair follicles resulting in a failure of hair regrowth. In addition, the stem cells were not fully activated after full thickness wounds were generated in VDR null skin under a low calcium diet to suppress compensation pathways. Cell proliferation was not fully induced in potential stem cells located in both IFE and hair follicles near the wounding edges, and re-epithelialization rate was delayed in VDR null skin. Gene expression profiling of the wounded skin (3 days after injury) indicated that β-catenin signaling was not fully induced in VDR null skin comparable to that observed in β-catenin null mice. The β-catenin target genes including Axin2 and cell cycle regulators involved in epidermal stem cell function were not induced in the edges of the wound of VDR null skin. These results demonstrated that VDR plays an essential role in hair cycling and wound healing processes through regulation of β-catenin signaling in epidermal stem cells and their progenies. n=3 CON and KO (each sample contain RNA isolated from wounded skins excised from 3 mice)
2015-07-31 | E-GEOD-68728 | biostudies-arrayexpress
Project description:The vitamin D receptor (VDR) regulates cell proliferation and differentiation including epidermal keratinocytes by modulating transcription of its target genes. We are investigating the role of VDR in epidermal stem cells and their progenies in the regeneration process of epidermis and hair in the skin. VDR null mice are utilized in which VDR is specifically deleted in keratin 14 (K14) expressing keratinocytes by Cre-lox strategy. The impact of VDR deletion was evaluated by comparison of VDR null mice with no cre littermate control mice. The VDR was abundantly expressed in potential epidermal stem cells including basal cells in interfollicular epidermis (IFE), and in CD34 expressing bulge keratinocytes in hair follicles. Gene expression profiles and subsequent pathway analysis of stem cell enriched keratinocyte populations revealed that the VDR deletion significantly suppressed β-catenin signaling as well as VDR signaling. The role of VDR in epidermal stem cells was studied during hair follicle cycling and wound healing processes. The epidermal stem cells were not appropriately stimulated by hair depilation, and did not reinitiate anagen in the hair follicles resulting in a failure of hair regrowth. In addition, the stem cells were not fully activated after full thickness wounds were generated in VDR null skin under a low calcium diet to suppress compensation pathways. Cell proliferation was not fully induced in potential stem cells located in both IFE and hair follicles near the wounding edges, and re-epithelialization rate was delayed in VDR null skin. Gene expression profiling of the wounded skin (3 days after injury) indicated that β-catenin signaling was not fully induced in VDR null skin comparable to that observed in β-catenin null mice. The β-catenin target genes including Axin2 and cell cycle regulators involved in epidermal stem cell function were not induced in the edges of the wound of VDR null skin. These results demonstrated that VDR plays an essential role in hair cycling and wound healing processes through regulation of β-catenin signaling in epidermal stem cells and their progenies. n=3 CON and KO (each sample contain RNA isolated from wounded or nonwounded skins excised from 3 mice)
2015-07-31 | E-GEOD-68727 | biostudies-arrayexpress
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