Gene expression profile of keloid tissue
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE2945 | GEO | 2005/07/16
SECONDARY ACCESSION(S): PRJNA92447
REPOSITORIES: GEO
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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:Transcriptional profiling of active keloid lesion and adjacent control normal skin tissue from human. Each control and lesion sample was derived from a matched individual.
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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:RNA sequencing has been performed to investigate the transcriptomic profile of keratinocyte derived from keloid and normal skin tissue. Keratinocytes of low passage (p2-4) were cultured onto T25 flasks until full confluence was reached. Keratinocytes were then harvested by trypsinization using 0.05% trypsin-EDTA and washed in Phosphate Buffered Saline (PBS). RNA was extracted using the RNeasy Mini kit protocol. Samples were then sent to the Australian Genome Research Facility (AGRF) where 1μg of RNA was submitted for next-generation sequencing. Once raw data returned, bioinformatics analyses were conducted. Through RNA-seq and bioinformatics analysis, 252 differentially expressed genes were identified in keloid keratinocytes compared to normal skin keratinocytes. Further gene ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) analyses revealed that changes in tight junctions and dysregulated response to viral infection were associated with keloid epithelia and may be linked to the disease. The results of the transcriptome analysis intimate that keloid derived keratinocytes exhibit an abnormal gene expression profile and the abnormalities in keloid keratinocytes may have an important role in keloid pathogenesis.
2021-10-06 | GSE185309 | 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: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.
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Project description:small non-codingRNA in Human keloid scar tissue and normal skin tissue
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Project description:We selected 3 pairs of keloid and normal skin matched by age and site of onset to observe the expression difference of small noncoding RNA
2022-01-19 | E-MTAB-11336 | biostudies-arrayexpress
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.
2007-11-26 | E-GEOD-7890 | biostudies-arrayexpress
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
2007-11-26 | GSE7890 | GEO