Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

GNPS - Influence of sex and disease stage on epidermal lipid profiles in SHARPIN-deficient mice

ABSTRACT: Skin is an essential organ that preserves the integrity of the body and the maintenance of lipid content and composition is essential for proper epidermal barrier function. SHANK-associated RH domain interacting protein-deficient mice spontaneously develop a chronic proliferative dermatitis with similarities to atopic dermatitis in humans. To learn about changes in the epidermal lipid-content in male and female mice during disease progression, we used 18 male and 18 female wild-type mice and 3 groups of littermates mice with dermatitis (6 male and 6 female each) divided according to the stage of disease: non-lesional, established and advanced. A mass-spectrometry strategy for biomarker discovery termed multiple-reaction monitoring-profiling was used to detect and monitor 1030 lipid ions present in the epidermis samples. Univariate analysis was performed to link lipids to disease stage in a sex-dependent or independent manner. An elastic-net regression model was built using the top 10 lipid features to predict disease progression. Individual samples were classified into their corresponding disease stage groups with an accuracy of 0.90 (95% CI:0.86, 0.93). Multiple-reaction monitoring-profiling paired with machine-learning identified predictive biomarkers of dermatitis in mice and may provide the basis for a molecular diagnostic approach to atopic dermatitis.

INSTRUMENT(S): 6410 Triple Quadrupole LC/MS

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Harm HogenEsch

PROVIDER: MSV000083884 | GNPS | Mon Jun 03 12:43:00 BST 2019

REPOSITORIES: GNPS

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Influence of sex and disease stage on epidermal lipid profiles in SHARPIN-deficient mice

Project description:Skin is an essential organ that preserves the integrity of the body and the maintenance of lipid content and composition is essential for proper epidermal barrier function. SHANK-associated RH domain interacting protein-deficient mice spontaneously develop a chronic proliferative dermatitis with similarities to atopic dermatitis in humans. To learn about changes in the epidermal lipid-content in male and female mice during disease progression, we used 18 male and 18 female wild-type mice and 3 groups of littermates mice with dermatitis (6 male and 6 female each) divided according to the stage of disease: non-lesional, established and advanced. A mass-spectrometry strategy for biomarker discovery termed multiple-reaction monitoring-profiling was used to detect and monitor 1030 lipid ions present in the epidermis samples. Univariate analysis was performed to link lipids to disease stage in a sex-dependent or independent manner. An elastic-net regression model was built using the top 10 lipid features to predict disease progression. Individual samples were classified into their corresponding disease stage groups with an accuracy of 0.90 (95% CI:0.86, 0.93). Multiple-reaction monitoring-profiling paired with machine-learning identified predictive biomarkers of dermatitis in mice and may provide the basis for a molecular diagnostic approach to atopic dermatitis.

2019-06-03 | MSV000083884 | MassIVE

Local and systemic changes in lipid profile as potential biomarkers for canine atopic dermatitis.

Project description:Lipids play a critical role in the skin as components of the epidermal barrier and as sig-naling molecules. Atopic dermatitis in dogs is associated with changes in the lipid composition of the skin, but whether these precede the onset of dermatitis or occur secondary to the dermatitis is unclear. We applied rapid lipid profiling mass spectrometry methods to skin and blood samples of dogs and determined changes following systemic treatment. Thirty control dogs and 30 atopic dogs with mild to moderate dermatitis were enrolled. Marked differences in lipid profiles were observed between control, nonlesional and lesional skin of dogs. Additionally, there were significant altera-tions in the lipid composition of the blood samples indicating systemic changes in lipid metabolism. Treatment with oclacitinib or lokivetmab resulted in a significant decrease of the disease clinical severity associated with changes in skin and blood lipids. A set of lipid features of the skin were selected as biomarkers that classified samples as control or atopic dermatitis with 95% accuracy, whereas blood lipids discriminated between control and atopic dogs with 82% accuracy. These data suggest that atopic dermatitis is a systemic disease and support the use of rapid lipid profiling to identify novel biomarkers.

2021-07-16 | MSV000087837 | MassIVE

comprehensive miRNA analysis of human atopic plasma

Project description:miRNAs are kown to be deeply involved in the progression of chronic inflammatory diseases. We comprehensively analyzed miRNAs in human plasma from AD(atopic dermatitis) and ACD(allergic conjunctival disease) patients. We performed a comprehensive human plasma miRNA analysis and identified significantly up-regulated miRNAs in both AD (atopic dermatitis) and ACD (allergic conjunctival disease).

2022-11-08 | GSE217232 | GEO

EGR1 increases the innervation density of epidermal sensory neurons via upregulation of ARTN in keratinocytes in atopic dermatitis

Project description:Atopic dermatitis (AD) is the chronic inflammatory skin disease accompanied with severe pruritus. To explore the roles of EGR1 in atopic dermatitis and the relationship between EGR1 and pruritus-scratching behavior, we used a atopic dermatitis-like mouse model driven by house dust mite (HDM) treatment in wild type and EGR1 KO mice, followed with RNA-sequencing analysis.

2024-01-15 | GSE214750 | GEO

Establishment of novel atopic dermatitis model by Nestin-cre mediated Ikk2 deficiency

Project description:To generate novel atopic dermatitis model, we used Nestin-cre mediated Ikk2FL/FL mice. Nestincre-mediated conditional knockout mice of Ikk2 gene were generated by crossing female Ikk2FL/FL mice to male Nestin-cre;Ikk2FL/+mice. Nestin-cre;Ikk2FL/FL mice spontaneously develop chronic AD-like skin inflammation and severe pruritus. We further performed Cap analysis of gene expression (CAGE) to elucidate transcriptional profiles in lesional skin of Nestin-cre;Ikk2FL/FL mice.

2020-01-26 | GSE109936 | GEO

Sonic Hedgehog signalling to T cells limits induction of chronic murine atopic dermatitis via Gli2-driven immune regulatory function

Project description:Hedgehog (Hh) proteins are morphogens which regulate embryonic development and adult tissue homeostasis, with distinct outcomes dependent on the strength and duration of their signals. We show that the Hh signalling pathway modulates the induction and pathology of mouse atopic dermatitis. Sonic hedgehog (Shh) and Hh pathway target genes were upregulated on induction of atopic dermatitis, and the Hh pathway was activated in skin T cells, showing that they respond in vivo to Hh signals secreted from the skin. Shh upregulation reduced skin inflammation in mice, whereas pharmacological Smoothened-inhibition reduced Shh upregulation and exacerbated skin pathology. Hh-signalling to T cells prevented skin inflammation on induction of dermatitis, while inhibition of Hh-mediated transcription in T cells substantially exacerbated the disease. RNA-sequencing analysis of skin CD4+ T cells from mice with chronic atopic dermatitis revealed decreased expression of immune regulatory genes in mice with conditional inhibition of Hh-mediated transcription in T cells, and increased expression of inflammatory and chemokine genes. In contrast, constitutive Hh mediated transcription in T cells led to increased expression of immune regulatory genes in skin CD4+ T cells from mice with chronic atopic dermatitis and protected against inflammation. Hh-mediated transcription in T cells resulted in increased regulatory T (Treg) cells in the periphery and skin of dermatitis-induced mice, and increased TGF-β expression, supporting their immunoregulatory phenotype, whereas, inhibition of T cell specific Hh-mediated transcription, resulted in impaired Treg function, which permitted progression of skin inflammation.

2021-07-14 | GSE117338 | GEO

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.

2017-05-01 | GSE96957 | GEO

Genome-wide analysis of gene expression in the cervical spinal cord of a mouse model of atopic dermatitis

Project description:Genome-wide analysis of gene expression in the cervical spinal cord of atopic dermatitis model mice was performed. Results provide important information for understanding of molecular mechanisms of the symptoms of atopic dermatitis.

2015-07-17 | GSE70114 | GEO

Watanabe2018_Simple markov model

Project description:Simple Markov model. There are 3 disease states: Healthy, Sick, and Dead, where the Dead state is terminal. The yearly transition probabilities are: Healthy to Dead: 0.01; Healthy to Sick: 0.2 for Male and 0.1 for Female; Sick to Healthy: 0.1; Sick to Dead: 0.3. The transition probability now depends on the cohort (Male or Female) and can be expressed as a function of a Boolean covariate Male. Initial conditions: Healthy = (50 Male, 50 Female), Sick = (0,0) and Dead = (0,0). Output: Number of men and women in each disease state for years 1-10.

2019-01-30 | MODEL1803120004 | BioModels

Genome-wide binding profile of the AhR transcription factor in keratinocytes

Project description:Atopic dermatitis is increasing worldwide, correlating with air pollutions. Various organic components of pollutants activate transcription factor AhR (aryl-hydrocarbon receptor). We have established AhR-CA mice, whose keratinocytes express constitutive-active AhR, and these mice developed atopic dermatitis-like frequent scratching and allergic inflammation. In this study we performed ChIP-seq analyses and identified keratinocyte-specific AhR target genes, including inflammatory cytokines Tslp and IL33, and neurotrophic factor Artemin. While AhR-CA mice exhibited epidermal hyperinnervation and alloknesis leading to hypersensitivity to pruritus, blockade of Artemin alleviated these phenotypes. AhR-CA mice showed scratching-induced barrier insufficiency and enhanced sensitization to epicutaneously-applied antigens, recapitulating human atopic dermatitis. Consistently, AhR activation and Artemin expression was detected in the epidermis of atopic dermatitis patients and keratinocytes exposed to air pollutants. Thus, AhR in keratinocytes senses the environmental stimuli and responds to them through moderating inflammation. We propose a mechanism in which air pollution induces atopic dermatitis through AhR activation.

2016-11-13 | GSE72455 | 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