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ABSTRACT: Time series integrative analysis of RNA-Seq and miRNA expression data reveals key biologic pathways during keloid formation

PROVIDER: PRJNA448679 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6937760_1.fastq.gz	Fastqsanger.gz
	SRR6937760_2.fastq.gz	Fastqsanger.gz
	SRR6937770_1.fastq.gz	Fastqsanger.gz
	SRR6937770_2.fastq.gz	Fastqsanger.gz
	SRR6937780_1.fastq.gz	Fastqsanger.gz

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Time series integrative analysis of RNA-Seq and miRNA expression data reveals key biologic pathways during keloid formation [miRNA]

Project description:Time series integrative analysis of RNA-Seq and miRNA expression data reveals key biologic pathways during keloid formation [miRNA]

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Time series integrative analysis of RNA-Seq and miRNA expression data reveals key biologic pathways during keloid formation

Project description:Time series integrative analysis of RNA-Seq and miRNA expression data reveals key biologic pathways during keloid formation

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Time series integrative analysis of RNA-Seq and miRNA expression data reveals key biologic pathways during keloid formation [RNA-seq]

Project description:Keloids represent a common form of exaggerated wound scarring that cause considerable morbidity. Moreover, there are limited data on molecular mechanisms underlying keloids and effective therapies are lacking. To gain new insight in the transcriptomic alterations of wound healing in keloid-prone individuals, we followed an integrative approach of RNA-Seq and miRNA expression data analysis in serial skin biopsies of the same site (baseline and six weeks after wounding) in keloid-prone (n=8) and healthy matched control individuals (n=6). Bioinformatic analysis identified 37 miRNAs and 1449 genes that are differentially expressed specifically in keloid-prone individuals during wound healing. Pathway enrichment analysis was undertaken in the RNA-Seq data and identified NOTCH signaling, MAPK signaling, and Toll-like receptor pathways to be altered in keloid-prone individuals after wounding. In addition, dysregulation of DNA repair, p53 signalling and metabolic pathways (RNA, protein, fructose, mannose and glycerophospholipid metabolism) was highlighted during keloid formation. Gene association network analysis demonstrated divergent average expression profiles of cytokine signaling genes, as well as lipid metabolism genes between keloid-prone and healthy individuals during wound healing. In summary, our study provides a comprehensive and integrative analysis of the keloid transcriptome and miRNAome and highlights biological pathways that feature during keloid formation.

2018-06-29 | GSE113619 | GEO

Time series integrative analysis of RNA-Seq and miRNA expression data reveals key biologic pathways during keloid formation [miRNA]

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Integrative Transcriptomic Profiling reveals Hepatic Stem-like Phenotype and Interplay of EMT and miR-200c in Intrahepatic Cholangiocarcinoma

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Project description:Keloids are fibroproliferative dermal tumors of unknown origin that are characterized by the overabundant accumulation of extracellular matrix (ECM) components. The mechanism of keloid formation has remained unclear because of a poor understanding of its molecular basis. In this study, the dermal ECM components of keloids were identified, and the pathological mechanism of keloid formation was characterized using large-scale, quantitative proteomic analyses of decellularized keloid biomatrix scaffolds. We identified a total of 267 dermal core ECM and ECM-associated proteins that were differentially expressed between patients with keloids and healthy controls. Skin mechanical properties, key pathways, and biological processes including protease activity, wound healing, and adhesion were disordered in keloids. The integrated network analysis of the upregulated ECM proteins revealed the involvement of estrogen signaling pathways in keloid formation. Our findings may improve the scientific basis of keloid treatment and provide new ideas for the establishment of keloid models.

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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.

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Gene profiling of keloid fibroblasts shows altered expression in multiple fibrosis-associated pathways

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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