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Effect of TWEAK or TGF-α on gene expression of primary human keratinocytes (PHKs)

ABSTRACT: Effect of TWEAK or TGF-α on gene expression of primary human keratinocytes (PHKs)

PROVIDER: PRJNA834055 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19033236.fastq.gz	Fastqsanger.gz
	SRR19033237.fastq.gz	Fastqsanger.gz
	SRR19033238.fastq.gz	Fastqsanger.gz
	SRR19033239.fastq.gz	Fastqsanger.gz
	SRR19033240.fastq.gz	Fastqsanger.gz

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Effect of TWEAK or TGF-α on gene expression of primary human keratinocytes (PHKs)

Project description:To investigate the transcriptome of TWEAK or TGF-α in the regulation of human primary keratinocytes We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 replicates at two different time points

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Transcriptomic Analysis of Human Epidermal Keratinocytes Stimulated with TWEAK, TNF and IL-17A

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Transcription profiling of primary mouse keratinocytes infected with Myc, MycV394D or control virus supernatants and treated with or without TGF beta 1 for 12 hours

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2005-12-20 | E-MEXP-497 | biostudies-arrayexpress

TWEAK mediates inflammation in experimental atopic dermatitis and psoriasis

Project description:Atopic dermatitis and psoriasis are driven by alternate type 2 and type 17 immune responses, but some proteins might be critical to both diseases. We show that a deficiency of the TNF superfamily molecule TWEAK (TNFSF12) in mice results in defective maintenance of atopic dermatitis-specific Th2 and psoriasis-specific Th17 cells in the skin, and impaired expression of disease-characteristic chemokines and cytokines, such as CCL17 and TSLP in atopic dermatitis, and CCL20 and IL-19 in psoriasis. The TWEAK receptor, Fn14, is upregulated in keratinocytes and dermal fibroblasts, and TWEAK induces these cytokines and chemokines alone and in synergy with the signature T helper cytokines of either disease, IL-13 and IL-17. Furthermore, subcutaneous injection of recombinant TWEAK into naïve mice induces cutaneous inflammation with histological and molecular signs of both diseases. TWEAK is therefore a critical contributor to skin inflammation and a possible therapeutic target in atopic dermatitis and psoriasis.

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Next Generation Sequencing Facilitates Quantitative Analysis of Primary Keratinocytes and OSM-treated Primary Keratinocytes Transcriptomes

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare transcriptome profiling (RNA-seq) between Primary Keratinocytes and OSM-treated Primary Keratinocytes Methods: mRNA profiles of Primary Keratinocytes and OSM-treated Primary Keratinocytes were generated by deep sequencing, in triplicate, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks.

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Next Generation Sequencing Facilitates Quantitative Analysis of Primary Keratinocytes and OSM-treated Primary Keratinocytes Transcriptomes

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of Primary Keratinocytes and OSM-treated Primary Keratinocytes Transcriptomes

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microRNA profiling of primary human keratinocytes and primary human dermal fibroblasts

Project description:In search for factors, overexpression of which in human dermal fibroblasts causes direct conversion to cells similar to keratinocytes, micro RNA expression profiles of human primary keratinocytes and human primary dermal fibroblasts are investigated. Skin samples obtained from 3 different sites of 1 subject were used for establishment of 3 primary keratinocytes and 3 primary dermal fibroblasts. Thus obtained 3 primary keratinocytes and primary dermal fibroblasts underwent micro RNA profiling.

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Project description:The study aims at illustrate novel role of TWEAK/Fn14 signaling in synapse function by combining electrophysiological and phosphoproteomic approaches. The results show that TWEAK acutely dampens basal synaptic transmission and plasticity through neuronal Fn14 and impacts the phosphorylation state of pre- and post-synaptic proteins in adult mouse hippocampal slices. Two models featuring synaptic deficits were used in the study. Blocking TWEAK/Fn14 signaling augments synaptic function in hippocampal slices from amyloid beta-overexpressing mice. After stroke, genetic or pharmacological inhibition of TWEAK/Fn14 signaling augments basal synaptic transmission and normalizes plasticity. Our data support a glial/neuronal axis that critically modifies synaptic physiology and pathophysiology in different contexts in the mature brain and may be a therapeutic target for improving neurophysiological outcomes.

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