Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Manually curated and harmonised transcriptomics datasets of psoriasis and atopic dermatitis patients.

ABSTRACT: We present manually curated transcriptomics data of psoriasis and atopic dermatitis patients retrieved from the NCBI Gene Expression Omnibus and EBI ArrayExpress repositories. We collected 39 transcriptomics datasets, deriving from DNA microarrays and RNA-Sequencing technologies, for a total of 1677 samples. We provide quality-checked, homogenised and preprocessed gene expression matrices and their corresponding metadata tables along with the estimated surrogate variables. These data represent a ready-made valuable source of knowledge for translational researchers in the dermatology field.

SUBMITTER: Federico A

PROVIDER: S-EPMC7555498 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Manually curated and harmonised transcriptomics datasets of psoriasis and atopic dermatitis patients.

Federico Antonio A Hautanen Veera V Christian Nils N Kremer Andreas A Serra Angela A Greco Dario D

Scientific data 20201013 1

We present manually curated transcriptomics data of psoriasis and atopic dermatitis patients retrieved from the NCBI Gene Expression Omnibus and EBI ArrayExpress repositories. We collected 39 transcriptomics datasets, deriving from DNA microarrays and RNA-Sequencing technologies, for a total of 1677 samples. We provide quality-checked, homogenised and preprocessed gene expression matrices and their corresponding metadata tables along with the estimated surrogate variables. These data represent a ...[more]

PMID: 33051456

Similar Datasets

Manually curated transcriptomics data collection for toxicogenomic assessment of engineered nanomaterials.

Project description:Toxicogenomics (TGx) approaches are increasingly applied to gain insight into the possible toxicity mechanisms of engineered nanomaterials (ENMs). Omics data can be valuable to elucidate the mechanism of action of chemicals and to develop predictive models in toxicology. While vast amounts of transcriptomics data from ENM exposures have already been accumulated, a unified, easily accessible and reusable collection of transcriptomics data for ENMs is currently lacking. In an attempt to improve the FAIRness of already existing transcriptomics data for ENMs, we curated a collection of homogenized transcriptomics data from human, mouse and rat ENM exposures in vitro and in vivo including the physicochemical characteristics of the ENMs used in each study.

| S-EPMC7870661 | biostudies-literature

Genomic imprinting in psoriasis and atopic dermatitis: A review.

Project description:Genomic imprinting is a genetic process where only one allele of a particular gene is expressed in a parent-of-origin dependent manner. Epigenetic changes in the DNA, such as methylation or acetylation of histones, are primarily thought to be responsible for silencing of the imprinted allele. Recently, global CpG methylation changes have been identified in psoriatic skin in comparison to normal skin, particularly near genes known to be upregulated in psoriasis such as KYNU, OAS2, and SERPINB3. Furthermore, imprinting has been associated with multi-chromosomal human disease, including diabetes and multiple sclerosis. This paper is the first to review the clinical and genetic evidence that exists in the literature for the association between imprinting and general skin disorders, including atopic dermatitis and psoriatic disease. Atopy was found to have evidence of imprinting on chromosomes 6, 11, 14, and 13. The ? subunit of the IgE receptor on chromosome 11q12-13 may be imprinted. Psoriatic disease may be related to imprinting effects on chromosome 6 for psoriasis and 16 for psoriatic arthritis.

| S-EPMC4679559 | biostudies-other

Aryl Hydrocarbon Receptor in Atopic Dermatitis and Psoriasis.

Project description:The aryl hydrocarbon receptor (AHR)/AHR-nuclear translocator (ARNT) system is a sensitive sensor for small molecular, xenobiotic chemicals of exogenous and endogenous origin, including dioxins, phytochemicals, microbial bioproducts, and tryptophan photoproducts. AHR/ARNT are abundantly expressed in the skin. Once activated, the AHR/ARNT axis strengthens skin barrier functions and accelerates epidermal terminal differentiation by upregulating filaggrin expression. In addition, AHR activation induces oxidative stress. However, some AHR ligands simultaneously activate the nuclear factor-erythroid 2-related factor-2 (NRF2) transcription factor, which is a master switch of antioxidative enzymes that neutralizes oxidative stress. The immunoregulatory system governing T-helper 17/22 (Th17/22) and T regulatory cells (Treg) is also regulated by the AHR system. Notably, AHR agonists, such as tapinarof, are currently used as therapeutic agents in psoriasis and atopic dermatitis. In this review, we summarize recent topics on AHR related to atopic dermatitis and psoriasis.

| S-EPMC6862295 | biostudies-literature

Microbe-host interplay in atopic dermatitis and psoriasis.

Project description:Despite recent advances in understanding microbial diversity in skin homeostasis, the relevance of microbial dysbiosis in inflammatory disease is poorly understood. Here we perform a comparative analysis of skin microbial communities coupled to global patterns of cutaneous gene expression in patients with atopic dermatitis or psoriasis. The skin microbiota is analysed by 16S amplicon or whole genome sequencing and the skin transcriptome by microarrays, followed by integration of the data layers. We find that atopic dermatitis and psoriasis can be classified by distinct microbes, which differ from healthy volunteers microbiome composition. Atopic dermatitis is dominated by a single microbe (Staphylococcus aureus), and associated with a disease relevant host transcriptomic signature enriched for skin barrier function, tryptophan metabolism and immune activation. In contrast, psoriasis is characterized by co-occurring communities of microbes with weak associations with disease related gene expression. Our work provides a basis for biomarker discovery and targeted therapies in skin dysbiosis.

| S-EPMC6795799 | biostudies-literature

Genetically programmed differences in epidermal host defense between psoriasis and atopic dermatitis patients.

Project description:In the past decades, chronic inflammatory diseases such as psoriasis, atopic dermatitis, asthma, Crohn's disease and celiac disease were generally regarded as immune-mediated conditions involving activated T-cells and proinflammatory cytokines produced by these cells. This paradigm has recently been challenged by the finding that mutations and polymorphisms in epithelium-expressed genes involved in physical barrier function or innate immunity, are risk factors of these conditions. We used a functional genomics approach to analyze cultured keratinocytes from patients with psoriasis or atopic dermatitis and healthy controls. First passage primary cells derived from non-lesional skin were stimulated with pro-inflammatory cytokines, and expression of a panel of 55 genes associated with epidermal differentiation and cutaneous inflammation was measured by quantitative PCR. A subset of these genes was analyzed at the protein level. Using cluster analysis and multivariate analysis of variance we identified groups of genes that were differentially expressed, and could, depending on the stimulus, provide a disease-specific gene expression signature. We found particularly large differences in expression levels of innate immunity genes between keratinocytes from psoriasis patients and atopic dermatitis patients. Our findings indicate that cell-autonomous differences exist between cultured keratinocytes of psoriasis and atopic dermatitis patients, which we interpret to be genetically determined. We hypothesize that polymorphisms of innate immunity genes both with signaling and effector functions are coadapted, each with balancing advantages and disadvantages. In the case of psoriasis, high expression levels of antimicrobial proteins genes putatively confer increased protection against microbial infection, but the biological cost could be a beneficial system gone awry, leading to overt inflammatory disease.

| S-EPMC2409155 | biostudies-literature

TWEAK mediates inflammation in experimental atopic dermatitis and psoriasis.

Project description:Atopic dermatitis (AD) and psoriasis are driven by alternate type 2 and type 17 immune responses, but some proteins might be critical to both diseases. Here we show that a deficiency of the TNF superfamily molecule TWEAK (TNFSF12) in mice results in defective maintenance of AD-specific T helper type 2 (Th2) and psoriasis-specific Th17 cells in the skin, and impaired expression of disease-characteristic chemokines and cytokines, such as CCL17 and TSLP in AD, 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 naive 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 AD and psoriasis.

| S-EPMC5493595 | biostudies-literature

Microarray transcriptome profiling of atopic dermatitis and psoriasis patients compared to healthy volunteers.

Project description:Characteization host-microbiome interactions in patients with allergic (model: atopic dermatitis) and autoimmune (model: psoriasis) diseases by integration of microarray transcriptome data with 16S microbial profiling. 6mm punch biopsies were collected from the skin of atopic dermatitis and psoriasis patients alongside healthy volunteers, and subjected to analysis using Affymetrix Human Gene ST 2.1 arrays.

2019-09-11 | E-MTAB-8149 | biostudies-arrayexpress

N6-methyladenosine (m6A) modification in patients with psoriasis or atopic dermatitis [MeRIPseq_Human]

Project description:We analyzed m6A modifications in skin lesions of patients with psoriasis or atopic dermatitis (AD). The results of this study will help to gain insight into the molecular basis of m6A modification in inflammatory skin diseases such as psoriasis or atopic dermatitis.

2024-08-20 | GSE268744 | GEO

ILDGDB: a manually curated database of genomics, transcriptomics, proteomics and drug information for interstitial lung diseases.

Project description:BackgroundInterstitial lung diseases (ILDs), a diverse group of diffuse lung diseases, mainly affect the lung parenchyma. The low-throughput 'omics' technologies (genomics, transcriptomics, proteomics) and relative drug information have begun to reshaped our understanding of ILDs, whereas, these data are scattered among massive references and are difficult to be fully exploited. Therefore, we manually mined and summarized these data at a database (ILDGDB, http://ildgdb.org/ ) and will continue to update it in the future.Main bodyThe current version of ILDGDB incorporates 2018 entries representing 20 ILDs and over 600 genes obtained from over 3000 articles in four species. Each entry contains detailed information, including species, disease type, detailed description of gene (e.g. official symbol of gene), and the original reference etc. ILDGDB is free, and provides a user-friendly web page. Users can easily search for genes of interest, view their expression pattern and detailed information, manage genes sets and submit novel ILDs-gene association.ConclusionThe main principle behind ILDGDB's design is to provide an exploratory platform, with minimum filtering and interpretation, while making the presentation of the data very accessible, which will provide great help for researchers to decipher gene mechanisms and improve the prevention, diagnosis and therapy of ILDs.

| S-EPMC7731518 | biostudies-literature

Atopic Dermatitis, Psoriasis and healthy control RNA-seq cohort

Project description:To gain a deeper understanding of the pathophysiology of AD, we conducted a large-scale transcriptomic study of AD with deeply-sequenced RNA-seq samples using long (125b) paired-end reads. By integrating deep sequencing-based skin transcriptome profiling with systems biology analysis, we are able to provide deep characterization for the expression signatures for AD, and by including psoriasis samples in the analysis, we can reveal the distinct molecular features of uninvolved and lesional skin of AD that have not been previously described.

2019-01-18 | GSE121212 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data