Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1047734 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27024207_1.fastq.gz | Fastqsanger.gz | |||
| SRR27024207_2.fastq.gz | Fastqsanger.gz | |||
| SRR27024208_1.fastq.gz | Fastqsanger.gz | |||
| SRR27024208_2.fastq.gz | Fastqsanger.gz | |||
| SRR27024209_1.fastq.gz | Fastqsanger.gz |
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Project description:OBJECTIVE To compare the effect of topical application PLCL/Fg dressing with alginate dressing (ConvaTec Ltd) when treating DFUs. DESIGN, SETTING, AND PARTICIPANTS A single-center, prospective, randomized, patient-blinded clinical trial was conducted from February 1, 2023, to November 16, 2023. The eligible patients with DFUs of 1 to 20 cm2 present for at least 1 month and with Wagner grade 1 or 2. They were randomized 1:1 to receive PLCL/Fg or control alginate dressing. In PLCL/Fg group, 10 wounds samples were got from five patients at the time of the first dressing application and 50% wound healing time point. The wound specimens were subjected to messenger RNA sequencing. INTERVENTIONS Participants received PLCL/Fg dressing 1 to 3 times per week or Alginate dressing 3 times per week for 12 weeks. MAIN OUTCOMES AND MEASURES Primary end point was the incidence of complete healing. Complete healing was defined as complete re-epithelialization of the ulcer bed and absence of secretion. Secondary end points were time to relevant 50% wound reduction, infection, treatment-associated adverse events, and the microenvironment changing during wound healing.
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Project description:Venous leg ulcers (VLU) represent a clinical challenge and impair the patient’s quality of life. Venous insufficiency is underlying the protracted healing. We report the protein expression pattern for biomarkers in VLU wound fluids and compare these with acute split-thickness wound fluids.
Fifty-seven patients with VLU were recruited and treated for 12 weeks with a protease-modulating polyacrylate wound dressing and a two-layer bandage compression system. Ten patients with acute wounds were followed for 21 days. Wound size decreased from 18.7 ± 12.3 cm2 to 11.75 ± 11.39 cm2 in the VLU cohort, 10 wounds healed completely. Relative wound area reduction reached 48.9% ± 51.9% at week 12. 61.4% of the patients achieved a relative wound area reduction of ≥40% and 50.9% a relative wound area reduction of ≥60%.
IL-1beta, TNF-alpha, and MMP9 concentration ranges were similar in VLU and acute wound fluids. Concentrations of S100A8, S100A9, neutrophil elastase, MMP2, and fibronectin were elevated in VLU wound fluids and decreased significantly in abundance after two weeks of treatment. The values remained low, yet, higher than those of acute wounds. Collagen (I) alpha1 abundance was higher in VLU wound fluids and not significantly regulated.
Our data show a robust healing response in venous leg ulcers treated with a protease-modulating polyacrylate wound dressing. The biomarker pattern in VLU wound fluids changed within the first two weeks and we speculate that this might reflect a decrease of STAT3 influence in the wound bed.
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Project description:Effective therapy of wounds is difficult, especially for chronic, non-healing wounds, and novel therapeutics are urgently needed. This challenge can be addressed with bioactive wound dressings providing a microenvironment and facilitating cell proliferation and migration, ideally incorporating actives which initiate and/or progress effective healing upon release. In this context, electrospun scaffolds loaded with growth factors emerged as promising wound dressings due to their biocompatibility, similarity to the extracellular matrix and potential for controlled drug release. In this study, electrospun core-shell fibers were designed composed of a combination of polycaprolactone and polyethylene oxide. Insulin, a proteohormon with growth factor characteristics, was successfully incorporated into the core and was released in a controlled manner. The fibers exhibited favorable mechanical properties and a surface guiding cell migration for wound closure in combination with a high uptake capacity for wound exudate. Biocompatibility and significant wound healing effects were shown in interaction studies with human skin cells. As a new approach, analysis of the wound proteome in treated ex vivo human skin wounds clearly demonstrated a remarkable increase in wound healing biomarkers. Based on these findings, insulin-loaded electrospun wound dressings bear a high potential as effective wound healing therapeutics overcoming current challenges in the clinics.
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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.
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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:Adalimumab, but neither etanercept nor certolizumab-pegol, has been reported to induce a wound healing profile in the circulation of patients with hidradenitis suppurativa (HS), a chronic inflammatory skin disease. However, the role of tumor necrosis factor alpha (TNF) inhibitors in cutaneous wound healing in vivo is still unclear. To examine and compare the efficacy of various TNF inhibitors in cutaneous wound healing in vivo, a human TNF knock-in Leprdb/db mouse model was established to model the impaired cutaneous wound healing as seen in HS. 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 these inhibitors in accelerating cutaneous wound healing. Taken together, these data revealed that TNF inhibitors exhibited differential levels of efficacy in accelerating cutaneous wound healing in the impaired wound healing model in vivo likely through distinct mechanisms of action related to the structure of the biologic or its ability to bind TNF.
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Project description:BRAF inhibitors are highly effective therapies for patients with BRAF V600 mutated metastatic melanoma. Patients who receive BRAF inhibitors develop a variety of hyper-proliferative skin conditions, whose pathogenic basis is the paradoxical activation of the mitogen-activated protein kinase (MAPK) pathway in BRAF wild-type cells. Most of these hyper-proliferative skin changes improve when a MEK inhibitor is co-administered, as a MEK inhibitor blocks paradoxical MAPK activation. We tested whether we could take advantage of the mechanistic understanding of the skin hyper-proliferative side effects of BRAF inhibitors to accelerate skin wound healing by inducing paradoxical MAPK activation. Here we show that the BRAF inhibitor vemurafenib accelerates human keratinocyte proliferation and migration by increasing ERK phosphorylation and cell cycle progression. Topical treatment with vemurafenib in two wound-healing models in mice accelerated cutaneous wound healing and improved the tensile strength of healing wounds through paradoxical MAPK activation; addition of a MEK inhibitor reversed the benefit of vemurafenib-accelerated wound healing. The same dosing regimen of topical BRAF inhibitor did not increase the incidence of cutaneous squamous cell carcinomas in mice even after the application of a carcinogen. Therefore, topical BRAF inhibitors may have clinical applications in accelerating the healing of skin wounds. Full depth incisional wound mice tissues with/without Vemurafenib treatment were sent for RNAseq analysis on day 2, 6 and 14
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