Schwann cells contribute to keloid formation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA751564 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15324500.fastq.gz | Fastqsanger.gz | |||
| SRR15324501.fastq.gz | Fastqsanger.gz | |||
| SRR15324502.fastq.gz | Fastqsanger.gz | |||
| SRR15324503.fastq.gz | Fastqsanger.gz | |||
| SRR15324504.fastq.gz | Fastqsanger.gz |
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Project description:Due to limited availability of proper models to study keloid development, the underlying pathomechanisms of this severe skin disease is still poorly understood. Here we performed single-cell sequencing of keloids and identified the occurrence of a so far unrecognized keloidal Schwann cell population, remaining in the scar tissue after wound healing. In contrast to normal skin, keloidal Schwann cells possess a repair-like phenotype and high cellular plasticity. Our data reveal that keloidal Schwann cells directly contribute to the formation of the extracellular matrix and affect M2 polarization of macrophages. Indeed, we show that macrophages in keloids predominantly display a M2 polarization and produce factors inhibiting Schwann cell differentiation. Our data suggest that this cross-talk contribute to the infinite growth of keloids and that targeting Schwann cells might represent a novel treatment option for keloids.
2022-03-16 | GSE181316 | GEO
Project description:Keloids represent a common form of exaggerated wound scarring that cause considerable morbidity. Moreover, there are limited data on molecular mechanisms underlying keloids and effective therapies are lacking. To gain new insight in the transcriptomic alterations of wound healing in keloid-prone individuals, we followed an integrative approach of RNA-Seq and miRNA expression data analysis in serial skin biopsies of the same site (baseline and six weeks after wounding) in keloid-prone (n=8) and healthy matched control individuals (n=6). Bioinformatic analysis identified 37 miRNAs and 1449 genes that are differentially expressed specifically in keloid-prone individuals during wound healing. Pathway enrichment analysis was undertaken in the RNA-Seq data and identified NOTCH signaling, MAPK signaling, and Toll-like receptor pathways to be altered in keloid-prone individuals after wounding. In addition, dysregulation of DNA repair, p53 signalling and metabolic pathways (RNA, protein, fructose, mannose and glycerophospholipid metabolism) was highlighted during keloid formation. Gene association network analysis demonstrated divergent average expression profiles of cytokine signaling genes, as well as lipid metabolism genes between keloid-prone and healthy individuals during wound healing. In summary, our study provides a comprehensive and integrative analysis of the keloid transcriptome and miRNAome and highlights biological pathways that feature during keloid formation.
2018-06-29 | GSE113620 | GEO
Project description:Keloids represent a common form of exaggerated wound scarring that cause considerable morbidity. Moreover, there are limited data on molecular mechanisms underlying keloids and effective therapies are lacking. To gain new insight in the transcriptomic alterations of wound healing in keloid-prone individuals, we followed an integrative approach of RNA-Seq and miRNA expression data analysis in serial skin biopsies of the same site (baseline and six weeks after wounding) in keloid-prone (n=8) and healthy matched control individuals (n=6). Bioinformatic analysis identified 37 miRNAs and 1449 genes that are differentially expressed specifically in keloid-prone individuals during wound healing. Pathway enrichment analysis was undertaken in the RNA-Seq data and identified NOTCH signaling, MAPK signaling, and Toll-like receptor pathways to be altered in keloid-prone individuals after wounding. In addition, dysregulation of DNA repair, p53 signalling and metabolic pathways (RNA, protein, fructose, mannose and glycerophospholipid metabolism) was highlighted during keloid formation. Gene association network analysis demonstrated divergent average expression profiles of cytokine signaling genes, as well as lipid metabolism genes between keloid-prone and healthy individuals during wound healing. In summary, our study provides a comprehensive and integrative analysis of the keloid transcriptome and miRNAome and highlights biological pathways that feature during keloid formation.
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Project description:The immune response is postulated to exert a pivotal role in the occurrence and progression of keloid. In recent years, the impact of the peripheral immune microenvironment on keloid has garnered significant attention in scholarly investigations exploring the underlying pathogenesis of this condition. In this study, we isolated CD45+ cells from keloid and normal scar dermis tissues by fluorescence activated cell sorting (FACS) and performed single-cell RNA sequencing analysis. Our results revealed the intricate cellular landscape of immune cells in keloid. We found that compared to normal scar tissue, the percentage of Th17 cells was significantly increased in keloid. Further functional studies revealed that Th17 cell promotes proliferation, migration and collagen expression of keloid fibroblast through IL17a. These findings will help us more thoroughly understand keloid pathogenesis and provide potential targets for keloid therapies.
2025-01-06 | GSE270438 | GEO
Project description:Keloid scars is a pathologic fibro-proliferative disorders of the skin, which exhibit abnormal phenotypes including fibroblasts proliferation and collagen deposits. There have been several treatments of keloids including conventional surgical therapies and adjuvant therapies, but a high recurrence rate of keloids was also observed after treatment. Quantitative proteomics approach has been proved an efficient approach to investigate pathological mechanism and novel biomarkers. In this study, we present a label-free quantitative proteomics analysis to explore differential protein expression profiles in normal skin and keloid scar tissues based on nano-liquid chromatography and tandem mass spectrometry (Nano-LC–MS/MS). The study results displayed a more comprehensive keloid protein expression landscape and provided novel pathological insight of keloid.
2023-03-11 | PXD029631 | Pride
Project description:Keloids are benign tumors of the dermis that form during a protracted wound healing process. Susceptibility to keloid formation occurs predominantly in people of African and Asian descent. The key alteration(s) responsible for keloid formation has not been identified and there is no satisfactory treatment for this disorder. The altered regulatory mechanism is limited to dermal wound healing, although several diseases characterized by an exaggerated response to injury are prevalent in individuals of African ancestry. We have observed a complex pattern of phenotypic differences in keloid fibroblasts grown in standard culture medium or induced by hydrocortisone. In this study Affymetrix-based microarray was performed on RNA obtained from fibroblasts cultured from normal scars and keloids grown in the absence and presence of hydrocortisone. We observed differential regulation of approximately 500 genes of the 38,000 represented on the Affymetrix chip. Of particular interest was increased expression of several IGF-binding and IGF-binding related proteins and decreased expression of a subset of Wnt pathway inhibitors and multiple IL-1-inducible genes. Increased expression of CTGF and IGFBP-3 was observed in keloid fibroblasts only in the presence of hydrocortisone. These findings support a role for multiple fibrosis-related pathways in the pathogenesis of keloids Keywords: cell-type comparison, drug treatment comparison Cell cultures were initiated from human biopsy material from normal dermal scars and keloids of adult males and females. Experimental cultures were derived from the first passage of cells thawed from liquid nitrogen. Cultures of fibroblasts from samples were grown with or without 1.5 micromolar hydrocortisone. RNA from each cell strain was isolated from three independent cell cultures and pooled, then run on an Affymetrix Human Genome U133 Plus 2.0 GeneChip.
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Project description:Comparison of keloid to normal tissue Keywords: examination of keloid tissue
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