Gene expression profile at single cell level of primary keloid fibroblasts treated with various radiotherapy modalities
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ABSTRACT:
PROVIDER: PRJNA1085306 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28264634_1.fastq.gz | Fastqsanger.gz | |||
| SRR28264634_2.fastq.gz | Fastqsanger.gz | |||
| SRR28264635_1.fastq.gz | Fastqsanger.gz | |||
| SRR28264635_2.fastq.gz | Fastqsanger.gz | |||
| SRR28264636_1.fastq.gz | Fastqsanger.gz |
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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.
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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.
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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:Aberrant production of extracellular matrix (ECM) from dermal fibroblasts drives fibrotic skin diseases, which significantly affect the quality of patients’ lives. Current treatment options for skin fibrosis remain limited or ineffective; therefore, new antifibrotic strategies are urgently needed. Gaining insights into molecular control of ECM production could lead to the identification of new therapeutic targets. Recent studies suggest Zinc Finger 469 (ZNF469) as a positive regulator for ECM production; however, its role in skin fibrosis has not been investigated. In this study, we found that knockdown of ZNF469 impaired proliferation, migration, and contraction in human dermal fibroblasts. More importantly, depletion of ZNF469 significantly caused a reduction in collagen production. RNA-sequence analysis of ZNF469-knockdown cells revealed significant suppression of several ECM genes and genes involved in the process of collagen biosynthesis, suggesting ZNF469 as a key regulator of ECM production. To find the clinical relevance, we examined expression of ZNF469 by reanalyzing public bulk and single-cell RNA-sequence data sets of hypertrophic scars and keloids as a representation of skin fibrosis. The RNA sequence of bulk tissues showed that hypertrophic scar and keloid tissues had higher levels of ZNF469 and that ZNF469 and ECM genes were positively correlated. Single-cell RNA sequence of keloid scars revealed restricted expression of ZNF469 in the fibroblast population. Further analysis of fibroblast subpopulations showed specific expression of ZNF469 in mesenchymal fibroblasts, a subpopulation that has been demonstrated to be crucial for collagen overexpression in keloids. Psuedotime analysis indicated ZNF469 as a pioneering factor to establish the mesenchymal fibroblast subpopulation. Supporting this finding, we observed downregulation of various mesenchymal fibroblast markers from our RNA sequence results of ZNF469-depleted dermal fibroblasts, suggesting ZNF469 as a crucial factor for maintaining mesenchymal phenotypes. Finally, to explore the therapeutic potential of ZNF469, we silenced it in human keloid fibroblasts and demonstrated that its depletion reduced proliferation, migration, contraction, and collagen production. Moreover, expression of key mesenchymal fibroblast markers was significantly downregulated in ZNF469-knockdown keloid fibroblasts. Together, we illustrated that ZNF469 promoted the ECM production in dermal fibroblasts and could serve as a novel target for treating skin fibrosis.
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