Bulk-cell RNA-seq analysis of early cutaneous wound healing in mouse
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB26375 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2532150.fastq.gz | Fastqsanger.gz | |||
| ERR2532151.fastq.gz | Fastqsanger.gz | |||
| ERR2532152.fastq.gz | Fastqsanger.gz | |||
| ERR2532153.fastq.gz | Fastqsanger.gz | |||
| ERR2532154.fastq.gz | Fastqsanger.gz |
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Project description:To study early-onset gene expression changes in cutaneous wound healing, 3 mm wounds were induced into the back skin of female wildtype C57BL/6 mice using a biopsy punch. Mice were sacrificed 2h, 6h or 24h post wound induction (PWI) and 1 - 1.5 mm of skin lining the wound edge was isolated and sequenced. The skin from the initial punch biopsy (0h PWI) was preserved and taken as a control sample to identify differentially expressed genes.
2018-07-31 | E-MTAB-6686 | biostudies-arrayexpress
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Project description:Comparative analysis between oral and cutaneous wound healing in humans using paired and sequential biopsies during the repair process.
2018-08-07 | GSE97615 | GEO
Project description:Adalimumab is the only FDA- and EMA-approved treatment for moderate-to-severe hidradenitis suppurativa (HS), suggesting that the mechanism of action of adalimumab is distinct in HS and may contribute to improved wound healing. We have demonstrated that adalimumab, but neither etanercept nor certolizumab-pegol, induces a wound healing profile in vitro, which may underlie the differences in efficacy between various anti-TNF agents. To examine and compare the efficacy of therapeutic TNF inhibitors in chronic cutaneous wound healing in vivo, a human TNF knock-in Leprdb/db mouse model was established. The vehicle group exhibited severe impairments in cutaneous wound healing. In contrast, adalimumab significantly accelerated healing, confirmed by both histologic assessment and a unique healing transcriptional profile. Moreover, adalimumab and infliximab showed similar levels of efficacy, but golimumab was less effective, along with etanercept and certolizumab-pegol. In line with histologic assessments, proteomics analyses from healing wounds exposed to various TNF inhibitors revealed distinct and differential wound healing signatures that may underlie the differential efficacy of therapeutic inhibitors in accelerating chronic wound healing.
2023-09-11 | PXD040275 | Pride
Project description:Proteases control complex tissue responses by modulating inflammation, cell proliferation and migration, and matrix remodeling. All these processes are orchestrated in cutaneous wound healing to restore the skin’s barrier function upon injury. Altered protease activity has been implicated in the pathogenesis of healing impairments, and proteases are important targets in diagnosis and therapy of this pathology. Global assessment of proteolysis at critical turning points after injury will define crucial events in acute healing that might be disturbed in healing disorders. As optimal biospecimens, wound exudates contain an ideal proteome to detect extracellular proteolytic events, are non-invasively accessible, and can be collected at multiple time points along the healing process from the same wound in the clinics. In this study, we applied multiplexed Terminal Amine Isotopic Labeling of Substrates (TAILS) to globally assess proteolysis in early phases of cutaneous wound healing. By quantitative analysis of proteins and protein N termini in wound fluids from a clinically relevant pig wound model, we identified more than 650 proteins and discerned major healing phases through distinctive abundance clustering of markers of inflammation, granulation tissue formation, and re-epithelialization. TAILS revealed a high degree of proteolysis at all time points after injury by detecting almost 1300 N-terminal peptides in ~450 proteins, most of which could not be assigned to known mature protein N termini. Quantitative positional proteomics mapped pivotal interdependent processing events in the blood coagulation cascade, detailed activating thrombin cleavages in vivo, and temporally discerned clotting and fibrinolysis during the healing process. Similarly, we found virtually all major cleavages in complement activation and inactivation and demonstrated time-dependent changes in the proteolytic potential of the wound milieu by detecting processing of complement C3 at distinct time points after wounding and by different proteases.
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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.
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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.
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Project description:Female sex hormones are beneficial effects for wound healing. However, till date, whether topical estrogen application can promote cutaneous wound healing in diabetes remains unclear. Therefore, the present study aimed to validate the effect of topical estrogen application on cutaneous wound healing in a type 2 diabetes db/db mice model. In total, 22 db/db female mice with type 2 diabetes and eight C57BL/6J female mice were subjected to two full-thickness wound injuries. The mice were divided into the db/db, db/db + estrogen, db/db + vehicle, and wild type (WT) groups. Wound healing was assessed until day 14. The db/db group had a significantly high wound area ratio (wound area/initial wound area) on days 3–14 and a significantly low re-epithelialization ratio on days 7 and 14. Moreover, their angiogenesis ratio was significantly low on day 7 and high on day 14. In contrast, compared with the db/db group, the db/db + estrogen group had a significantly lower wound area ratio on days 1–14 and angiogenesis ratio on day 14, thereby indicating early withdrawal of new blood vessels, as well as a significantly higher re-epithelialization ratio on days 7 and 14 and Ym1+ M2 macrophage/macrophage ratio on day 7. Moreover, microarray analysis showed that the top 10 upregulated or downregulated genes in the db/db group were reversed by estrogen treatment, particularly on day 14, in comparison with the WT group. Thus, topical estrogen application reduced the wound area, promoted re-epithelialization and angiogenesis, and increased the number of M2 macrophages in mice with type 2 diabetes. Furthermore, it improved the differential regulation of genes in db/db mice. Therefore, such treatment can enhance cutaneous wound healing in female mice with type 2 diabetes.
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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