Expression data from keloid fibroblasts.
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ABSTRACT:
PROVIDER: PRJNA1253766 | ENA |
REPOSITORIES: ENA
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Project description:Keloids are benign fibroproliferative tumours resulting from skin damage such as trauma, burns or surgery. Keloids are more prevalent in populations with darkly pigmented skin. Links between skin pigmentation and vitamin D production have been established and some studies indicate involvement of vitamin D signalling in keloid pathology. This study assessed the impact of paricalcitol (a selective vitamin D signalling activator) on fibroblasts derived from keloid and normal skin, to further investigate the role and potential clinical relevance of vitamin D signalling in keloid pathology. Analysis of keloid and normal skin tissue using immunohistochemistry demonstrated a significant reduction of nuclear vitamin D receptor (VDR) in keloid tissue. After treatment with paricalcitol, nuclear VDR was increased in both keloid and normal fibroblasts. RNA sequencing of normal fibroblasts treated with paricalcitol demonstrated significant changes in gene expression, with many upregulated genes identified to have anti-fibrotic effects. However, paricalcitol failed to alter gene expression in Keloid fibroblasts. To investigate this further, we performed RNA sequencing of normal and keloid fibroblasts and found that retinoid-X receptor α (RXRα), a key binding partner of VDR required for downstream transcriptional activation, is significantly downregulated in keloid fibroblasts. Our results indicate that paricalcitol can effectively activate VDR translocation to the nucleus but is unable to effect change at the transcriptional level in keloid fibroblasts, most likely due to the reduced expression of RXRα. This suggests Vitamin D signalling may be aberrant in keloids, and that supplementation with Vitamin D alone would likely be ineffective in restoring signalling. Keywords: Keloid, Vitamin D receptor, Paricalcitol, Retinoid-X receptor α
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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: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.
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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
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