Ontology highlight
ABSTRACT:
PROVIDER: PRJNA764368 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15972309_1.fastq.gz | Fastqsanger.gz | |||
| SRR15972309_2.fastq.gz | Fastqsanger.gz | |||
| SRR15972310_1.fastq.gz | Fastqsanger.gz | |||
| SRR15972310_2.fastq.gz | Fastqsanger.gz | |||
| SRR15972311_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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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
2024-12-03 | GSE282479 | GEO
Project description:Background:Keloid (KL) is a common benign skin tumor. KL is typically characterized by significant fibrosis and an intensive inflammatory response. Therefore, a comprehensive understanding of the interactions between cellular inflammation and fibrotic cells is essential to elucidate the mechanisms driving the progression of KL and to develop therapeutics. Objective: Investigate the transcriptome landscape of inflammation and fibrosis in keloid scars. Methods: In this paper, we performed transcriptome sequencing and microRNA (miRNA) sequencing on unselected live cells from six human keloid tissues and normal skin tissues to elucidate a comprehensive transcriptome landscape. In addition, we used single-cell RNA sequencing (scRNA-seq) analysis to analyze intercellular communication networks and enrich fibroblast populations in two additional keloid and normal skin samples to study fibroblast diversity. Results: By RNA sequencing and a miRNA-mRNA-PPI network analysis, we identified miR-615-5p and miR-122b-3p as possible miRNAs associated with keloids, as they differed most significantly in keloids. Similarly, COL3A1, COL1A2, THBS2, TNC, IGTA, THBS4, TGFB3 as genes with significant differences in keloid may be associated with keloid development. Using single-cell RNA sequencing data from 24086 cells collected from normal or keloid, we report reconstructed intercellular signaling network analysis and aggregation to modules associated with specific cell subpopulations at the cellular level for keloid alterations. Conclusions: Our multitranscriptomic dataset delineates inflammatory and fibro heterogeneity of human keloids, underlining the importance of intercellular crosstalk between inflammatory cells and fibro cells and revealing potential therapeutic targets.
2024-09-30 | GSE237753 | GEO
Project description:Keloid tissue: active keloid lesion vs. adjacent normal skin tissue
| PRJNA354398 | ENA
Project description:Keloids are dermal fibroproliferative skin disorders caused by abnormal wound healing, resulting in impaired skin function and aesthetic defects. Abnormal fibroblast proliferation and excessive collagen deposition are involved in keloid formation. This study investigated the role of fibroblast differentiation in keloid development. Single-cell and bulk RNA sequencing data of keloids were comprehensively analyzed, and 25 clinically relevant differentially expressed fibroblast-differentiation-related genes (DEFDRGs) were identified. Based on DEFDRGs, a keloid diagnostic classification system comprising three subtypes was constructed, indicating that DEFDRGs could serve as therapeutic targets. Additionally, multiple microarray datasets, protein sequencing data, and immunohistochemical analyses of key markers in clinical keloid samples were used for further verification. In conclusion, this study established a molecular classification of keloids based on fibroblast differentiation, contributing to the further understanding of keloid pathogenesis and providing new insights for diagnosis and treatment.
2025-10-06 | PXD066833 | Pride
Project description:Background:Keloid (KL) is a common benign skin tumor. KL is typically characterized by significant fibrosis and an intensive inflammatory response. Therefore, a comprehensive understanding of the interactions between cellular inflammation and fibrotic cells is essential to elucidate the mechanisms driving the progression of KL and to develop therapeutics. Objective: Investigate the transcriptome landscape of inflammation and fibrosis in keloid scars. Methods: In this paper, we performed transcriptome sequencing and microRNA (miRNA) sequencing on unselected live cells from six human keloid tissues and normal skin tissues to elucidate a comprehensive transcriptome landscape. In addition, we used single-cell RNA sequencing (scRNA-seq) analysis to analyze intercellular communication networks and enrich fibroblast populations in two additional keloid and normal skin samples to study fibroblast diversity. Results: By RNA sequencing and a miRNA-mRNA-PPI network analysis, we identified miR-615-5p and miR-122b-3p as possible miRNAs associated with keloids, as they differed most significantly in keloids. Similarly, COL3A1, COL1A2, THBS2, TNC, IGTA, THBS4, TGFB3 as genes with significant differences in keloid may be associated with keloid development. Using single-cell RNA sequencing data from 24086 cells collected from normal or keloid, we report reconstructed intercellular signaling network analysis and aggregation to modules associated with specific cell subpopulations at the cellular level for keloid alterations. Conclusions: Our multitranscriptomic dataset delineates inflammatory and fibro heterogeneity of human keloids, underlining the importance of intercellular crosstalk between inflammatory cells and fibro cells and revealing potential therapeutic targets.
2024-09-30 | GSE237754 | GEO
Project description:Background:Keloid (KL) is a common benign skin tumor. KL is typically characterized by significant fibrosis and an intensive inflammatory response. Therefore, a comprehensive understanding of the interactions between cellular inflammation and fibrotic cells is essential to elucidate the mechanisms driving the progression of KL and to develop therapeutics. Objective: Investigate the transcriptome landscape of inflammation and fibrosis in keloid scars. Methods: In this paper, we performed transcriptome sequencing and microRNA (miRNA) sequencing on unselected live cells from six human keloid tissues and normal skin tissues to elucidate a comprehensive transcriptome landscape. In addition, we used single-cell RNA sequencing (scRNA-seq) analysis to analyze intercellular communication networks and enrich fibroblast populations in two additional keloid and normal skin samples to study fibroblast diversity. Results: By RNA sequencing and a miRNA-mRNA-PPI network analysis, we identified miR-615-5p and miR-122b-3p as possible miRNAs associated with keloids, as they differed most significantly in keloids. Similarly, COL3A1, COL1A2, THBS2, TNC, IGTA, THBS4, TGFB3 as genes with significant differences in keloid may be associated with keloid development. Using single-cell RNA sequencing data from 24086 cells collected from normal or keloid, we report reconstructed intercellular signaling network analysis and aggregation to modules associated with specific cell subpopulations at the cellular level for keloid alterations. Conclusions: Our multitranscriptomic dataset delineates inflammatory and fibro heterogeneity of human keloids, underlining the importance of intercellular crosstalk between inflammatory cells and fibro cells and revealing potential therapeutic targets.
2024-09-30 | GSE237752 | GEO
Project description:Genome wide DNA methylation profiling of normal skin and keloid samples. The Illumina Infinium 450k Human DNA methylation Beadchip v1.1 was used to obtain DNA methylation profiles across approximately 485577 CpGs in keloid and normal samples. Samples included 6 normal skin, 6 Keloid. Bisulphite converted DNA from the 12 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip v1.1
2014-04-02 | E-GEOD-56420 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of normal skin and keloid samples. The Illumina Infinium 450k Human DNA methylation Beadchip v1.1 was used to obtain DNA methylation profiles across approximately 485577 CpGs in keloid and normal samples. Samples included 6 normal skin, 6 Keloid.
2014-04-02 | GSE56420 | GEO
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: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