Keloid Transcriptome
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ABSTRACT:
PROVIDER: PRJNA901908 | ENA |
REPOSITORIES: ENA
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Project description:Eevaluation of intra- and inter-keloid fibroblast heterogeneity by analyzing their gene expression using transcriptomic analysis
2023-11-15 | GSE218007 | GEO
Project description:Keloids are wounding-induced fibroproliferative human tumor–like skin scars of complex genetic makeup and poorly defined pathogenesis. Fibroblasts are the principal mediator of fibroproliferative disorders. To reveal dynamic epigenetic and transcriptome changes of keloid fibroblasts, a vertical study from RNA-seq and ATAC-seq analyses followed by in vivo confirmation of candidate molecule expression and subsequent functional testing was carried out using an early passage, freshly isolated keloid fibroblast cell strain and its paired normal control. These keloid fibroblasts produce keloid-like scars in a plasma clot-based skin equivalent humanized keloid animal model. RNA-seq analysis reveals that Hepatic fibrosis is the most significant pathway followed by Wnt–b-catenin signaling, TGF-b signaling, regulation of the EMT pathway, the STAT3 pathway, and adherens junction signaling. ATAC-seq analysis shows that STAT3 signaling is the most active pathway in keloid fibroblasts, followed by Wnt signaling (Wnt5) and regulation of the EMT pathway. Immunohistochemistry confirms that activated STAT3, (Tyr705 phospho-STAT3) and/or b-catenin are upregulated in dermal fibroblasts of keloid clinical specimens and mature keloid skin equivalent implants from the humanized mouse model compared to the normal control. The effect of STAT3 signaling on keloid fibroblast collagen expression was further tested in plasma clot-based skin equivalents using Cucurbitacin I, a selective JAK2/STAT3 inhibitor. A non-linear dose response of Cucurbitacin I was observed in collagen type I expression indicating a likely role of STAT3 signaling pathway in keloid pathogenesis. This work also demonstrates the utility of the recently established humanized keloid mouse model in exploring the mechanism of keloid formation.
2020-01-11 | GSE125022 | 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:Comparison of keloid to normal tissue Keywords: examination of keloid tissue
2005-07-16 | GSE2945 | GEO
Project description:Keloid disease (KD) is a fibroproliferative cutaneous tumour characterised by heterogeneity, excess collagen deposition and aggressive local invasion. Normal and keloid scar tissues were analysed with a site-specific in situ approach through combined laser capture microdissection, as well as whole tissue biopsy and monolayer cell culture techniques.
2017-12-07 | E-MTAB-4945 | biostudies-arrayexpress
Project description:Comparison of keloid to normal tissue One sample for each type of tissue examined
2010-07-01 | E-GEOD-2945 | biostudies-arrayexpress
Project description:Keloids are scars that extend beyond original wounds and are resistant to treatment. In order to improve understanding of the molecular basis of keloid scarring, we have assessed the genomic profiles of keloid fibroblasts and keratinocytes. Skin and scar tissues were obtained for isolation of primary keratinocytes and fibroblasts. Keloid scars were excised from patients undergoing scar excision surgery, normal skin samples were isolated from patients undergoing elective plastic surgery. Primary culters were prepared for keratinocytes and fibroblasts, and were harvested for analysis up to passage three. Nine keloid scars, for adjacent non-lesional keloid skin samples, and three normal skin samples were obtained and cultured. RNA was isolated using RNeasy, and quality verified using an Agilent 2100 Bioanalyzer. Labeling and hybridization to Affymetrix Human Gene 1.0 ST microarray chips was performed by the Vanderbilt Genome Sciences Resource at Vanderbilt University Medical Center.
2013-05-28 | E-GEOD-44270 | biostudies-arrayexpress
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:Fibrosis is vaguely described as connective tissue deposition that can be excessive in pathological conditions. This suggests a quantitative spectrum of fibrosis wherein there can be more or less extracellular matrix (ECM), which in the context of a repairing skin wound could reflect the range from normal scar to keloid. This depiction, however, does not encompass the potential qualitative differences between normal and pathological scars. In keloids, the markedly different physical (hard and dense) and histological (hyalinization) characteristics compared to normal scars indicate an altered and inappropriate matrix, rather than simply too much. With this quantitative discovery-based proteomics we provide a thorough molecular description of keloid lesions relative to normal scars, which is an essential step towards our understanding of this problem.
2019-12-03 | PXD015057 | Pride
Project description:To further explore the expression of circular RNAs in keloid，we have completed the Arraystar Human circRNA Array V2 analysis of the 8 samples，including 4 patients-derived keloid dermal fibroblasts and 4 normal dermal fibroblasts.
2022-02-23 | GSE184097 | GEO