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UCHL1 aggravates skin fibrosis through an IGF-1-induced AKT/mTOR/ HIF-1α pathway in keloid

ABSTRACT: UCHL1 aggravates skin fibrosis through an IGF-1-induced AKT/mTOR/ HIF-1α pathway in keloid

PROVIDER: PRJNA869096 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21026561_1.fastq.gz	Fastqsanger.gz
	SRR21026561_2.fastq.gz	Fastqsanger.gz
	SRR21026562_1.fastq.gz	Fastqsanger.gz
	SRR21026562_2.fastq.gz	Fastqsanger.gz
	SRR21026563_1.fastq.gz	Fastqsanger.gz

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UCHL1 aggravates skin fibrosis through an IGF-1-induced AKT/mTOR/ HIF-1α pathway in keloid

Project description:To investigate the function of UCHL1 in keloids, we established primary dermal fibroblasts in which the target gene has been overexpressed by lentiviral transfection.

2022-11-21 | GSE211150 | GEO

Hypoxia and HIF-1α Regulate Collagen Production in Keloids

Project description:Keloids are reactive or spontaneous fibroproliferative dermal tumors characterized by the exaggerated and uncontrolled accumulation of extracellular collagen. Current approaches to mitigate keloidogenesis are largely procedural in nature. However, a better understanding of its biological drivers may lead to novel targeted treatments for keloids. Through whole-genome expression analysis, we found that a HIF-1α transcriptional footprint is preferentially upregulated (activation score=2.024; p=1.05E-19) in keloid fibroblasts (KFs) compared to normal dermal fibroblasts (NFs). We verified that HIF-1α protein is more strongly expressed in keloid specimens compared to normal skin (p=0.035) and that hypoxia (1% O2) leads to increased collagen, especially in the extracellular compartment. Collagen levels were uniformly reduced by selective HIF-1α inhibitor CAY10585. Our results indicate that collagen secretion may be intimately linked to a hypoxic microenvironment within keloid tumors and that HIF-1α blockade could be a novel avenue of treatment for these tumors.

2020-02-22 | GSE145725 | GEO

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.

2007-11-26 | E-GEOD-7890 | biostudies-arrayexpress

Genes regulated by UCHL1 in ovarian cancer cells

Project description:UCHL1 is related to apoptosis and proliferation in cancers and we sought to identify genes regulated by UCHL1

2013-01-30 | GSE43884 | GEO

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

2007-11-26 | GSE7890 | GEO

Genes regulated by UCHL1 in ovarian cancer cells

Project description:UCHL1 is related to apoptosis and proliferation in cancers and we sought to identify genes regulated by UCHL1 UCHL1 was knocked down in A2780 (A2780-shUCHL1). A2780-shUCHL1 and A2780-control were cultured in RPMI and total RNA was extracted and hybridizated on Affymetrix.GeneChip.HG-U133_Plus_2

2013-01-30 | E-GEOD-43884 | biostudies-arrayexpress

Keloid Transcriptome

Project description:Keloid Transcriptome

| PRJNA901908 | ENA

Quantitative proteomic analysis of keloid scars and normal skin tissues

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.

2023-03-11 | PXD029631 | Pride

Gene expression profile of keloid tissue

Project description:Comparison of keloid to normal tissue Keywords: examination of keloid tissue

2005-07-16 | GSE2945 | GEO

site-specific gene expression profiling in keloid disease

Project description:Keloid disease (KD) is a fibroproliferative cutaneous tumour characterised by heterogeneity, excess collagen deposition and aggressive local invasion. Normal and keloid scar tissues were analysed with a site-specific in situ approach through combined laser capture microdissection, as well as whole tissue biopsy and monolayer cell culture techniques.

2017-12-07 | E-MTAB-4945 | biostudies-arrayexpress

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