Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from mouse skin fibroblasts in homeostasis, inflammation and cancer

ABSTRACT: Expression data from mouse skin fibroblasts in homeostasis, inflammation and cancer

PROVIDER: PRJNA657027 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Expression data from mouse skin fibroblasts in homeostasis, inflammation and cancer

Project description:Fibroblasts are highly heterogenous and can exhibit distinct phenotypes depending on their activation state. To evaluate the specific phenotype of fibroblasts involved in inflammation versus wound-induced skin tumorigenesis, a genome-wide expression study was performed comparing gene expression profiles of ‘normal’, ‘inflammatory’ and ‘papilloma-associated’ fibroblasts.

2021-02-08 | GSE156197 | GEO

Gene expression profile at single cell level of fibroblasts from untreated (UT) and imiquimod (IMQ)-induced mouse skin.

Project description:We used single-cell RNA sequencing (scRNA-seq) to analyze the heterogeneity of dermal fibroblasts in homeostasis and skin inflammation.

2022-06-01 | GSE205020 | GEO

Skin inflammation

Project description:IL-12 protects from psoriasiform skin inflammation

| PRJEB15422 | ENA

Keratinocyte glucocorticoids enable local immune resilience to preserve skin homeostasis.

Project description:Endogenous glucocorticoids (GCs) are pivotal in controlling inflammation. Keratinocyte-derived GCs contribute to local skin homeostasis as deletion of the GC-producing enzyme 11β-hydroxylase (Cyp11b1) in keratinocytes exacerbated skin inflammation. Since local tamoxifen-induced knockout (KO) induction may contribute to skin irritation, we implemented intraperitoneal injections to induce a systemic skin GC depletion preventing experimental skin irritation in order to reveal the importance of skin GC in steady-state. Both, local and systemic skin GC deficiency models exhibited reduced skin GC levels and increased migration of skin antigen-presenting cells to draining lymph nodes. However, systemic skin GC ablation did not result in pronounced skin inflammation as seen in local model. Interestingly, systemic skin GC deficiency elevated systemic inflammatory markers and provoked adrenal GC synthesis. RNA sequencing of keratinocytes revealed distinct gene expression patterns between local and systemic KOs. Local skin GC ablation showed a stronger inflammatory and apoptotic response, while systemic skin GC deficiency triggered several compensatory regulatory pathways, mitigating extensive skin inflammation. These findings underscore the critical role of local GCs in skin immune resilience against minor skin irritations and highlight the interplay between skin and adrenal GC levels.

2024-08-01 | GSE271160 | GEO

Raw RNAseq data of HSV-1-infected mouse skin fibroblasts

Project description:Raw RNAseq data of HSV-1-infected mouse skin fibroblasts

| PRJNA498021 | ENA

Inflammation and tumor susceptibility in skin cancer

Project description:This SuperSeries is composed of the following subset Series: GSE12248: Genetic architecture of murine skin inflammation and tumor susceptibility GSE21247: Network Analysis of Skin Tumor Progression Identifies a Rewired Genetic Architecture Affecting Inflammation and Tumor Susceptibility (carcinomas) GSE21263: Network Analysis of Skin Tumor Progression Identifies a Rewired Genetic Architecture Affecting Inflammation and Tumor Susceptibility (papillomas) GSE26273: Network Analysis of Skin Tumor Progression Identifies a Rewired Genetic Architecture Affecting Inflammation and Tumor Susceptibility (aCGH) Refer to individual Series

2010-12-22 | E-GEOD-21264 | biostudies-arrayexpress

Early Life Inflammation Primes a Th2-Fibroblast Niche in Skin

Project description:Inflammation early in life can prime the local immune milieu of peripheral tissues, causing lasting changes in immunologic tone that confer disease protection or susceptibility. The cellular and molecular mechanisms that incite changes in immune tone in many nonlymphoid tissues remain largely unknown. We find that time-limited neonatal inflammation induced by transient reduction of neonatal regulatory T cells (Tregs) causes a dramatic dysregulation of subcutaneous tissue in murine skin, accompanied by the selective accumulation of Th2 cells within a distinct microanatomic niche. Th2 cells are maintained into adulthood through interactions with a fibroblast population in skin fascia that we refer to as Th2-interacting fascial fibroblasts (TIFFs), which expand in response to Th2 cytokines to form subcutaneous fibrous bands. Activation of the Th2-TIFF niche by neonatal inflammation primes skin for altered reparative responses to wounding. We further identify fibroblasts in healthy human skin expressing the TIFF transcriptional signature and find these cells at high levels in eosinophilic fasciitis, an orphan disease characterized by inflammation and fibrosis of the skin fascia. Taken together, these data define a novel Th2 niche in skin, functionally characterize a disease-associated fibroblast population, and suggest a mechanism of immunologic priming whereby inflammation early in life creates networks between adaptive immune cells and stromal cells, establishing an immunological set-point in tissues that is maintained throughout life.

2021-10-01 | GSE183031 | GEO

Skin & Pancreas chronic inflammation versus Normal Skin & Pancreas

Project description:Skin & Pancreas chronic inflammation versus Normal Skin & Pancreas

| PRJNA857740 | ENA

Epigenetic modules governing skin epidermal homeostasis [neonate skin epidermis]

Project description:Epigenetic modules governing skin epidermal homeostasis [neonate skin epidermis]

| PRJNA808402 | ENA

Skin & Pancreas chronic inflammation versus Normal Skin & Pancreas

Project description:To find which signaling is activated in chronic inflammation, we tried to induce chronic skin and pancreas inflammation compared to normal skin and pancreas.

2024-03-01 | GSE207956 | 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