Metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA506988 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR8247580_1.fastq.gz | Fastqsanger.gz | |||
| SRR8247580_2.fastq.gz | Fastqsanger.gz | |||
| SRR8247590_1.fastq.gz | Fastqsanger.gz | |||
| SRR8247590_2.fastq.gz | Fastqsanger.gz |
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Project description:Diabetic foot ulcers (DFUs) are a devastating complication of diabetes. To better understand the molecular mechanisms and cell types implicated in DFU healing, we used NanoString’s GeoMx Digital Spatial profiling platform on DFU tissue sections and compared gene expression of areas within the same ulcer as well as between patients who in 12 weeks following surgery healed their DFU (Healers, N=2) vs those who did not (Non-Healers, N=2).
2021-10-28 | GSE166120 | GEO
Project description:Objective: This study aims to investigate the diversity of fibroblasts present in diabetic ulcers and their impact on the wound healing process, as well as to evaluate the effectiveness of Platelet-Rich Plasma (PRP) therapy in the management of diabetic ulcers. Methodology: The single-cell dataset GSE165816 from the GEO database was utilized to analyze DFU-healer and DFU-nonhealer samples in order to evaluate variations in fibroblasts. Functional characteristics of fibroblasts were investigated through analyses of cell communication, transcription factors, and pseudotime analysis. Additionally, a diabetic ulcer rat model was established to compare the therapeutic effects of PRP, followed by histological and transcriptomic sequencing analyses. Result: Single-cell sequencing analysis identified a greater abundance of fibroblasts in the group of diabetic foot ulcer (DFU) patients who exhibited healing. The findings from biological informatics analysis emphasized the critical role of fibroblasts in the wound healing process. Treatment with PRP notably enhanced wound healing in diabetic ulcers in rats, and transcriptomic analysis indicated that gene expression levels post-PRP treatment resembled those of the non-diabetic ulcer group, with a strong association to fibroblasts. Conclusion: Fibroblasts are essential in the process of healing diabetic ulcers, as certain transcription factors have the potential to facilitate wound closure. PRP therapy has been shown to enhance the healing process in diabetic ulcer rat models, possibly through the modulation of gene expression and the promotion of extracellular matrix arrangement. This research offers novel insights and potential therapeutic approaches for managing diabetic ulcers.
2024-11-11 | GSE280992 | GEO
Project description:Diabetic foot ulcers (DFUs) are a devastating complication of diabetes. In order to identify systemic and local factors associated with DFU healing, we examined the cellular landscape of DFUs by single-cell RNA-seq analysis of foot and forearm skin specimens, as well as PBMC samples, from 10 non-diabetic subjects, and 17 diabetic patients, 11 with, and 6 without DFU. Our analysis shows enrichment of a unique inflammatory fibroblast population in DFU patients with healing wounds. The patients with healing DFUs also depicted enrichment of macrophages with M1 polarization, as opposed to more M2 macrophages in non-healing wounds. These findings were verified using Immunohistochemistry and Spatial Transcriptomics.
2021-11-01 | GSE165816 | GEO
Project description:We show that a combinatorial upregulation of SOX2 and hyperglycemia in cutaneous keratinocytes triggers a pro-healing signature and increased neutrophil chemoattraction, putatively by Ccr2, Ccr5, and Csf3r signaling. Neutrophil depletion and deregulation through the TREM1/FOXM1 pathway are directly implicated in diabetic foot ulcer (DFU) pathophysiology. Our results highlight the role of neutrophil recruitment in wound healing and can be used to explore potential therapeutic targets for DFUs in patients.
2024-07-22 | GSE266638 | GEO
Project description:Diabetes Mellitus (DM) is a chronic, severe disease rapidly increasing in incidence and prevalence and is associated with numerous complications. Patients with DM are at high risk of developing diabetic foot ulcers (DFU) that often lead to lower limb amputations, long term disability, and a shortened lifespan. Despite this, the effects of DM on human foot skin biology are largely unknown. Thus, the focus of this study was to determine whether DM changes foot skin biology predisposing it for healing impairment and development of DFU. Foot skin samples were collected from 20 patients receiving corrective foot surgery and, using a combination of multiple molecular and cellular approaches we performed comparative analyses of non-ulcerated non-neuropathic diabetic foot skin (DFS) and healthy non-diabetic foot skin (NFS). MicroRNA (miR) profiling of laser captured epidermis and primary dermal fibroblasts from both DFS and NFS samples identified 5 miRs de-regulated in the epidermis of DFS though none reached statistical significance. MiR-31-5p and miR-31-3p were most profoundly induced. Although none were significantly regulated in diabetic fibroblasts, miR-29c-3p showed a trend of up-regulation, which was confirmed by qPCR in a prospective set of 20 skin samples. Gene expression profiling of full thickness biopsies identified 36 de-regulated genes in DFS (>2 fold-change, unadjusted p-value ≤ 0.05). Of this group, three out of seven tested genes were confirmed by qPCR: SERPINB3 was up-regulated whereas OR2A4 and LGR5 were down-regulated in DFS. However no morphological differences in histology, collagen deposition, and number of blood vessels or lymphocytes were found. No difference in proliferative capacity was observed by quantification of Ki67 positive cells in epidermis. These findings suggest DM causes only subtle changes to foot skin. Since morphology, mRNA and miR levels were not affected in a major way, additional factors, such as neuropathy, vascular complications, or duration of DM, may further compromise tissue’s healing ability leading to development of DFUs.
2015-05-01 | GSE68185 | GEO
Project description:Diabetes Mellitus (DM) is a chronic, severe disease rapidly increasing in incidence and prevalence and is associated with numerous complications. Patients with DM are at high risk of developing diabetic foot ulcers (DFU) that often lead to lower limb amputations, long term disability, and a shortened lifespan. Despite this, the effects of DM on human foot skin biology are largely unknown. Thus, the focus of this study was to determine whether DM changes foot skin biology predisposing it for healing impairment and development of DFU. Foot skin samples were collected from 20 patients receiving corrective foot surgery and, using a combination of multiple molecular and cellular approaches we performed comparative analyses of non-ulcerated non-neuropathic diabetic foot skin (DFS) and healthy non-diabetic foot skin (NFS). MicroRNA (miR) profiling of laser captured epidermis and primary dermal fibroblasts from both DFS and NFS samples identified 5 miRs de-regulated in the epidermis of DFS though none reached statistical significance. MiR-31-5p and miR-31-3p were most profoundly induced. Although none were significantly regulated in diabetic fibroblasts, miR-29c-3p showed a trend of up-regulation, which was confirmed by qPCR in a prospective set of 20 skin samples. Gene expression profiling of full thickness biopsies identified 36 de-regulated genes in DFS (>2 fold-change, unadjusted p-value ≤ 0.05). Of this group, three out of seven tested genes were confirmed by qPCR: SERPINB3 was up-regulated whereas OR2A4 and LGR5 were down-regulated in DFS. However no morphological differences in histology, collagen deposition, and number of blood vessels or lymphocytes were found. No difference in proliferative capacity was observed by quantification of Ki67 positive cells in epidermis. These findings suggest DM causes only subtle changes to foot skin. Since morphology, mRNA and miR levels were not affected in a major way, additional factors, such as neuropathy, vascular complications, or duration of DM, may further compromise tissue’s healing ability leading to development of DFUs.
2015-05-01 | GSE68184 | GEO
Project description:Diabetes Mellitus (DM) is a chronic, severe disease rapidly increasing in incidence and prevalence and is associated with numerous complications. Patients with DM are at high risk of developing diabetic foot ulcers (DFU) that often lead to lower limb amputations, long term disability, and a shortened lifespan. Despite this, the effects of DM on human foot skin biology are largely unknown. Thus, the focus of this study was to determine whether DM changes foot skin biology predisposing it for healing impairment and development of DFU. Foot skin samples were collected from 20 patients receiving corrective foot surgery and, using a combination of multiple molecular and cellular approaches we performed comparative analyses of non-ulcerated non-neuropathic diabetic foot skin (DFS) and healthy non-diabetic foot skin (NFS). MicroRNA (miR) profiling of laser captured epidermis and primary dermal fibroblasts from both DFS and NFS samples identified 5 miRs de-regulated in the epidermis of DFS though none reached statistical significance. MiR-31-5p and miR-31-3p were most profoundly induced. Although none were significantly regulated in diabetic fibroblasts, miR-29c-3p showed a trend of up-regulation, which was confirmed by qPCR in a prospective set of 20 skin samples. Gene expression profiling of full thickness biopsies identified 36 de-regulated genes in DFS (>2 fold-change, unadjusted p-value ≤ 0.05). Of this group, three out of seven tested genes were confirmed by qPCR: SERPINB3 was up-regulated whereas OR2A4 and LGR5 were down-regulated in DFS. However no morphological differences in histology, collagen deposition, and number of blood vessels or lymphocytes were found. No difference in proliferative capacity was observed by quantification of Ki67 positive cells in epidermis. These findings suggest DM causes only subtle changes to foot skin. Since morphology, mRNA and miR levels were not affected in a major way, additional factors, such as neuropathy, vascular complications, or duration of DM, may further compromise tissue’s healing ability leading to development of DFUs.
2015-05-01 | GSE68183 | GEO
Project description:Diabetes Mellitus (DM) is a chronic, severe disease rapidly increasing in incidence and prevalence and is associated with numerous complications. Patients with DM are at high risk of developing diabetic foot ulcers (DFU) that often lead to lower limb amputations, long term disability, and a shortened lifespan. Despite this, the effects of DM on human foot skin biology are largely unknown. Thus, the focus of this study was to determine whether DM changes foot skin biology predisposing it for healing impairment and development of DFU. Foot skin samples were collected from 20 patients receiving corrective foot surgery and, using a combination of multiple molecular and cellular approaches we performed comparative analyses of non-ulcerated non-neuropathic diabetic foot skin (DFS) and healthy non-diabetic foot skin (NFS). MicroRNA (miR) profiling of laser captured epidermis and primary dermal fibroblasts from both DFS and NFS samples identified 5 miRs de-regulated in the epidermis of DFS though none reached statistical significance. MiR-31-5p and miR-31-3p were most profoundly induced. Although none were significantly regulated in diabetic fibroblasts, miR-29c-3p showed a trend of up-regulation, which was confirmed by qPCR in a prospective set of 20 skin samples. Gene expression profiling of full thickness biopsies identified 36 de-regulated genes in DFS (>2 fold-change, unadjusted p-value ≤ 0.05). Of this group, three out of seven tested genes were confirmed by qPCR: SERPINB3 was up-regulated whereas OR2A4 and LGR5 were down-regulated in DFS. However no morphological differences in histology, collagen deposition, and number of blood vessels or lymphocytes were found. No difference in proliferative capacity was observed by quantification of Ki67 positive cells in epidermis. These findings suggest DM causes only subtle changes to foot skin. Since morphology, mRNA and miR levels were not affected in a major way, additional factors, such as neuropathy, vascular complications, or duration of DM, may further compromise tissue’s healing ability leading to development of DFUs. foot skin biopsies obtained from diabetic and non-diabetic people were thoroughly washed in DMEM supplemented with 2× Penicillin/Streptomycin/Fungizone, and gentamicin (50mg/L). After, the epidermis was removed from specimens, the dermis was finely minced and placed in 12-well plates. For the establishment of fibroblast cultures, DMEM (Life Technologies) supplemented with 10% FBS, HEPES (1.9mg/ml), streptomycin (100 μg/ml), penicillin (100 U/ml), and Fungizone Antimycotic (0.25 µg/mL) was used. RNA was isolated from cells (passage 1 or 2) using miRNeasy Mini Kit (QIAGEN). miR expression profiles of DFF and NFF fibroblasts were generated by nanoString nCounter miR Expression Assays (NanoString Technologies, Seattle, WA, USA) and analyzed using nSolver2.0 software following manufacturer's instructions. Data were normalized to gene controls included in the assays.
2015-05-01 | E-GEOD-68185 | biostudies-arrayexpress
Project description:We investigate the changes between diabetic and non-diabetic wound healing process in chronic foot ulcer.
2023-10-24 | GSE245703 | GEO