Expression data from keloid fibroblasts.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1253766 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
Project description:Keloid Fibroblasts (KFs) scRNA seq
| PRJNA1066740 | ENA
Project description:Hypoxic areas and a metabolic shift toward glycolysis are common features of keloids. However, the roles and underlying molecular mechanisms of these features in keloid pathogenesis remain largely unknown.
2025-04-26 | GSE295249 | GEO
Project description:Keloids comprise an inflammatory fibroproliferative skin disorder characterized by excessive scarring. Fibroblasts play a pivotal role in skin fibrosis, exhibiting heightened collagen deposition. To investigate the molecular drivers of excessive collagen deposition in keloid, we compared the transcriptome of keloids and adjacent normal skin which demonstrated significant shifts towards bone and cartilage lineages in keloids, along with RUNX2, a key regulator of osteogenic and chondrogenic differentiation, notably upregulated. We then confirmed elevated levels of RUNX2 protein and phosphorylated RUNX2 in keloid tissue and fibroblasts compared to normal skin and normal dermal fibroblasts. To delve into how RUNX2 overexpression could contribute to keloids pathogenesis, we performed siRNA-mediated knockdown of RUNX2 in keloid fibroblasts followed by mRNA-sequencing. The results revealed significant downregulation of collagen genes COL11A1, COL5A3, COL15A1, and COL6A6, in knock-down vs. control groups along with GO enrichment analysis showing perturbation of genes involved in collagen and ECM organization. Further functional studies utilizing Runx2-knockout mice confirmed downregulation of these collagen genes along with reduced dermis thickness and reduced total dermal collagen in Runx2-knockout vs. Runx2- wild mice. These findings underscore the critical contribution of RUNX2 to collagen remodeling in keloid and provide potential therapeutic target.
2025-09-10 | GSE293677 | GEO
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
2024-12-03 | GSE282479 | GEO
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:RUNX2 regulates aberrant collagen gene expression in keloid fibroblasts
| PRJNA1245486 | ENA
Project description:This study investigated the effects of extracellular matrix (ECM) rigidty on gene expression patterns in normal dermal fibroblasts (NDFs) and keloid dermal fibroblasts (KDFs). Cells were cultured on collagen coated polyacrylamide hydrogels with elastic moduli mimicking normal skin (8 kPa) or keloid scar tissue (214 kPa), and changes in gene expression were profiled using next-generation RNA-sequencing. Differential gene expression analysis identified overall significant differences in gene expression between the NDF and KDF populations. Despite high levels of inter-patient heterogeneity in the KDF samples, further principal components analysis revealed a subset of genes (PC5) that were specifically regulated by ECM rigidity. Gene set enrichment analysis of the PC5 genes identified classic pathways associated with mechanotransduction, including Hippo Signalling and Regulation of the Actin Cytoskeleton, as well as genes associated with the Autophagy pathway. Additional in vitro studies and human tissue staining confirmed the biomechanical regulation of autophagic flux in NDFs and KDFs and differential remodelling of the lysosome in KDFs and keloid scars. Together, these findings implicate autophagy and lysosomal remodelling as biomechanically dysregulated pathways in keloid fibroblasts, and these mechanisms may contribute to scar pathogenesis.
2023-11-02 | GSE246562 | GEO
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
Project description:Here, we report that the knockdown of POSTN in fibroblasts leads to disruption in keloid inflammation. Moreover, molecules and pathway associated with extracellular matrix formation were impaired in POSTN-deficient fibroblasts. Therefore, our study highlights an indispensable role of POSTN in the pathogenesis of keloids.
2025-09-10 | GSE307210 | GEO