Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Basophils play a protective role in the recovery of skin barrier function from mechanical injury in mice

ABSTRACT: Mechanical skin injury promote an acute inflammation that impact the skin barrier function. The mechanisms to restore skin barrier function are not fully understood

ORGANISM(S): Mus musculus

PROVIDER: GSE252966 | GEO | 2024/02/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Basophils play a protective role in the recovery of skin barrier function from mechanical injury in mice

Project description:Basophils play a protective role in the recovery of skin barrier function from mechanical injury in mice

| PRJNA1063331 | ENA

Development of gene expression signatures for barrier recovery phase in epidermis from acute barrier disruption

Project description:The skin barrier consists of multiple lipid-enriched layers. Sodium lauryl sulfate is a well-known substance that can disrupt the skin barrier. The mechanisms underlying the barrier repair process, especially the influence of topical sodium lauryl sulfate treatment in the barrier recovery phase remain unresolved. To understand the process of reconstruction of the intercellular lipid layer of the skin after acute barrier disruption by sodium lauryl sulfate treatment in vivo.

2023-01-01 | GSE146969 | GEO

Molecular and Mechanical Signatures Contributing to Epidermal Differentiation and Barrier Formation

Project description:Formation of the skin barrier requires rapid proliferation coupled with differentiation and stratification of the embryonic epidermis. Basal progenitors give rise to progeny throughout development – first to intermediate cells, a transient proliferative suprabasal cell population, and later to spinous cells. Neither the function nor the differentiation trajectory of intermediate cells has been documented. We generated transcriptomes of intermediate and spinous cells and identified specific markers that distinguish these two populations. Further, we found that intermediate cells express a subset of genes in common with granular cells of the epidermis – the terminal living cell type that helps establish the barrier. Lineage tracing revealed that most intermediate cells directly transition to granular cells without expressing markers specific to spinous cells, thus revealing a distinct lineage pathway leading to granular fate. In addition to their transcriptional similarities, intermediate and granular cells both had hallmarks of increased actomyosin contractility. We found that rather than simply lying downstream of cell fate pathways, contractility was sufficient to suppress spinous fate and promote granular gene expression. Together, these data establish the molecular and mechanical characteristics of the developing epidermis that allow this tissue to rapidly develop barrier activity.

2025-05-01 | GSE295753 | GEO

Molecular and Mechanical Signatures Contributing to Epidermal Differentiation and Barrier Formation

Project description:Molecular and Mechanical Signatures Contributing to Epidermal Differentiation and Barrier Formation

| PRJNA1256298 | ENA

NLRP10 Maintains Epidermal Homeostasis by Promoting Keratinocyte Survival and P63-Dependent Differentiation and Barrier Function

Project description:Atopic dermatitis (AD) is a common chronic inflammatory skin disorder characterized by disrupted epidermal barrier function and aberrant immune responses. Despite recent developments in new treatments for AD, there are still unmet needs for the disease management due to its complex and multifactorial nature. Recent genome-wide association studies (GWAS) have identified NLRP10 as an AD susceptible gene. However, the physiological role of NLRP10 in skin homeostasis and its relevance to AD are unknown. Here we show that NLRP10 promotes keratinocyte survival and facilitates epidermal differentiation and barrier function. Mechanistically, NLRP10 limits cell death by preventing the recruitment of caspase-8 onto the death inducing signaling complex and inhibiting its subsequent activation. NLRP10 also stabilizes p63, the master regulator of keratinocyte differentiation, to drive proper keratinocyte differentiation and to reinforce the barrier function. Importantly, NLRP10 is downregulated in AD skin samples. Our findings underscore NLRP10 as a key player in atopic dermatitis pathogenesis, highlighting NLRP10 as a potential target for therapeutic intervention to restore skin barrier function and homeostasis in AD.

2024-10-17 | GSE264616 | GEO

Keratins control Nrf2 by regulating mitochondrial activity and barrier composition / Keratin-dependent TSLP expression suggests a link between skin blistering and atopic disease

Project description:The epidermal barrier protects the body against mechanical injury, infection and dehydration. The respective contribution of type I and type II keratins which form the major cytoskeleton in epidermal keratinocytes in barrier formation and stress protection is incompletely understood. Here, we reveal a novel mechanism by which keratins control anti-oxidant responses through barrier-dependent and cell-autonomous mechanisms. Mice lacking the entire type I (KtyI) or type II (KtyII) keratin gene clusters suffer from distinct prenatal barrier defects. Comparative transcriptome profiling identifies essential cornified envelope components and reveals strong upregulation of the bZIP transcription factor Nrf2 in situ. Isolated keratinocytes from both strains of mice show elevated mitochondrial oxygen consumption and Nrf2 activity, decreased upon keratin re-expression. We propose a model in which keratins control mitochondria-derived oxidative stress via Nrf2 activation. Our findings reveal major contributions of keratins to chronic inflammation and autoimmune disorders. Total RNA obtained from E18.5 embryo back skin from typeI and II keratin knockout compared with respective wild type.

2016-03-26 | E-GEOD-79590 | biostudies-arrayexpress

Targeted therapies restore skin barrier function and associated proteomics in atopic dermatitis

Project description:Background: Atopic dermatitis (AD) is characterized by skin barrier dysfunction. The impact of targeted therapies on skin barrier function and associated barrier protein changes remains not fully identified. Objective: To investigate the skin barrier function and proteomics in AD before and after different targeted therapies. Method: 15 healthy controls and 29 adult patients with moderate-to-severe AD were enrolled. AD patients were randomized into two groups. One group received dupilumab (N = 14) and the other received abrocitinib (N = 15). Clinical assessments and skin barrier parameters (transepidermal water loss [TEWL] and hydration) were measured at baseline, 4 weeks, and 12 weeks of treatment. Skin tape strips were collected for four-dimensional data-independent acquisition-based proteomics. Results: Both therapies improved skin barrier function, with abrocitinib showing greater effects on decreasing TEWL in the non-lesional skin. The proteomic analysis identified 1237 lesional and 785 non-lesional differentially expressed proteins (DEPs) between AD patients and healthy controls, especially in pathways related to ceramide metabolism, neurobiology, and keratinocyte biology. Treatment with abrocitinib resulted in more DEPs and significantly upregulated proteins associated with the epidermal barrier while downregulating immunological and itch-related proteins. It also increased key barrier proteins (filaggrin-2 and loricrin) in lesional skin, which was not shown in the dupilumab group. Both treatments regulated specific proteins in non-lesional skin, such as grancalcin and phospholipase D3. Conclusion: The study suggests that both targeted therapies improve the skin barrier function in AD, but they have different effects on barrier proteins, with abrocitinib having stronger effects.

2025-04-19 | PXD055561 | Pride

Traumatic Brain Injury Induces Early Barrier Protective Responses in Incisional Skin Wounds Accelerating Cutaneous Wound Healing

Project description:Though Traumatic Brain Injury (TBI) and skin trauma often occur together, it is unresolved whether TBI changes healing of skin wounds. We here explored whether TBI impacts on the sequence of events during skin wound healing. Incisional skin wounds from mice subjected to TBI were assessed employing unbiased transcriptome analysis and immunostaining. Transcriptome analysis at day 1 after combined trauma detects a significant enrichment of genes involved in macrophage and T cell recruitment and activation in contrast to skin wounds without TBI. At day 7 after combined trauma, genes in pathways of re-epithelialization including cornification and keratinization and of anti-inflammatory responses were highly enriched. These findings were confirmed by immunostaining with increased re-epithelialisation and cornification and an increased number of macrophages and T cells resolving inflammation. Moreover, the number of dermal myofibroblasts are highly increased in skin wounds after combined trauma. Collectively, TBI enforces an unprecedented defence response with an early onset of enhanced immunity, faster epidermal barrier formation, and a myofibroblast driven acceleration of wounds closure, all together likely counteracting systemic infection.

2025-09-03 | GSE288594 | GEO

Hair follicles modulate skin barrier function

Project description:We generated KA mutant mice (Krt14-CreERT + ABCA12-flox/flox) and controls (ABCA12-flox/flox) that enabled us to assess the effects of deleting a critical barrier gene, ABCA12, in the skin epidermis following tamoxifen treatment. These studies identified numerous differentially expressed genes (DEGs) upon barrier disruption/ABCA12 deletion, including compensatory upregulation of genes involved with epidermal differentiation and barrier function. Overall, this data-set provides a global view of molecular changes that occur in adult mouse skin following barrier perturbation.

2024-05-20 | GSE254889 | GEO

Hair follicles modulate skin barrier function

Project description:Hair follicles modulate skin barrier function

| PRJNA1072231 | ENA