Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome profiling of lesional skin from 3-week-old Tg.hKLK5 mice

ABSTRACT: Transgenic mice over-experssing human KLK5 (Tg.hKLK5) in the epidermis develop an inflammatory skin phenotype resembling Netherton syndrome. To characterize the skin inflammation phenotype of this mouse model at the molecular level, we collected back skin samples from young mice at three weeks of age, when the skin phenotype is most severe.

ORGANISM(S): Mus musculus

PROVIDER: GSE224673 | GEO | 2024/02/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcriptome profiling of lesional skin from neonate Spink5 constitutive knock-out mice

Project description:Spink5 constitituve knock-out mice mimic the disease features of Netherton syndrome but die within several hours after birth due to severe skin barrier defect. To characterize the skin barrier and skin inflammation phenotype of this mouse model at the molecular level, we collected back skin samples from mice shortly after their birth.

2024-02-05 | GSE224674 | GEO

Transcriptome profiling of lesional skin from Spink5 conditional knock-out mice

Project description:We generated a viable mouse model of Netherton syndrome by conditional ablation of Spink5 gene in the epidermis. To characterize this model at the molecular level, we induced Spink5 deletion in young adult mice and collected lesional skin samples for transcriptome analyses.

2024-02-05 | GSE224280 | GEO

Transcriptome profiling of lymph nodes from Spink5 conditional knock-out mice.

Project description:We generated a viable mouse model of Netherton syndrome by conditional ablation of Spink5 gene in the epidermis. To study the systemic inflammation phenotype of this mouse model at the molecular level, we induced Spink5 deletion in the skin of young adult mice and collected inguinal lymph nodes for transcriptome analyses.

2024-02-05 | GSE224409 | GEO

IκBζ-deficient epidermis mediates systemic autoimmune inflammation via skin dysbiosis.

Project description:Skin microbiota affect systemic inflammation through mechanisms that have not been completely elucidated. We previously demonstrated that keratinocyte-specific IκBζ-deficient mice spontaneously develop autoimmune inflammation resembling human Sjögren syndrome. In this study, we examined how IκBζ-deficient epidermis dictates systemic autoimmune inflammation onset. To examine if IκBζ-deficient keratinocytes are susceptible to apoptotic stimuli in a steady state, we performed microarray analysis of untreated murine back epidermis. Data indicate that IκBζ-deficient epidermis is susceptible to environment antigens through apoptosis-related gene upregulation

2022-08-11 | GSE165515 | GEO

A molecular signature for rejuvenation characterizes lesional and non lesional skin following Metvix treatment in Actinic Keratosis patients.

Project description:Actinic keratoses (AK) are proliferations of pre-neoplastic keratinocytes in the epidermis that are the result of cumulative ultraviolet (UV) radiations from sun exposure. Lesions are commonly found on sites of sun-exposed skin such as the face, balding scalp, and back of the hand. AKs may present on a patient as a few detectable lesions and 5-10% of them are susceptible to transform into SCC. In contrast, Organ Transplant Recipients (OTR) are of increasing risk at developing cancers as a consequence of long-term immunosuppressive therapy. The molecular changes that occur in lesional and perilesional skin of OTR patients 18 weeks following of PDT with topical MAL treatment were investigated to better understand the effect of the therapeutic intervention on the AK lesions. Our data show the complete normalization of the skin biology in the treated areas, i. e restoration of normal proliferation related gene profiles, and correction of aberrantly expressed cancer associated genes. We were also able to uncover a transcriptional signature of a rejuvenation effect induced by MAL-PDT in photodamaged skin opening new avenues in the use of PTD for treating photodamaged skin and field cancerized areas.

2018-06-15 | GSE90643 | GEO

Connective tissue regeneration dynamics persistently alter epithelial dynein DNAH10 expression - DNAH10 overexpression in psoriatic lesional epidermis

Project description:The objective of this study was to investigate how active dermal connective tissue composition dynamics affect long term protein expression in the epidermis. After surgically removing damaged skin to its full thickness at the site of a deep burn in ten patients, we randomized three adjacent test areas within the wounds to receive either: 1) no dermal component as control, 2) a permanent artificial dermal matrix or 3) a temporary dressing to induce formation of granulation tissue. Each area was then covered with an autologous superficial healty skin transplant as the epidermal indicator. One year later, biopsy samples were taken from each site. The epidermis and dermis were selectively microdissected by laser-capture from cut tissue biopsy sections, and analyzed using untargeted non-labelled quantitative proteomics.

2020-05-26 | PXD010852 | Pride

Transcription profiling by array of epidermal shave samples taken from lesional and non-lesional skin from German atopic dermatitis patients and from healthy skin from German controls

Project description:Epigenetic alterations are increasingly recognized as mechanisms for disease-associated changes in genome function and important risk factors for complex diseases. The epigenome differs between cell types and so far has been characterized in few human tissues only. In order to identify disease-associated DNA methylation differences for atopic dermatitis (AD), we investigated DNA from whole blood, T cells, B cells, as well as lesional and non-lesional epidermis from AD patients and healthy controls. To elicit functional links, we examined epidermal mRNA expression profiles. No genome-wide significant DNA methylation differences between AD cases and controls were observed in whole blood, T cells, and B cells, and, in general, intra-individual differences in DNA methylation were larger than interindividual differences. However, striking methylation differences were observed between lesional epidermis from patients and healthy control epidermis for various CpG sites, which partly correlated with altered transcript levels of genes predominantly relevant for epidermal differentiation and innate immune response. Significant DNA methylation differences were discordant in skin and blood samples, suggesting that blood is not an ideal surrogate for skin tissue. Our pilot study provides preliminary evidence for functionally relevant DNA methylation differences associated with AD, particularly in the epidermis, and represents a starting point for future investigations of epigenetic mechanisms in AD. Total RNA obtained from 7 patients from non-lesional skin, 12 patients from lesional skin and 14 controls from healthy skin

2014-08-26 | E-GEOD-60709 | biostudies-arrayexpress

Gene expression patterns induced by a transient switch-on of ROS production in mouse skin

Project description:Gene expression signatures induced by transient ROS production were characterized in both mouse back skin and tail epidermis samples. A transient in situ ROS production in the tissue was activated by an adapted photodynamic treatment, using methyl aminolevulinate as a metabolic precursor of endogenous Protoporphyrin IX. Gene expression in skin samples was measured 48 h after the photodynamic treatment. Experimental groups included: [1] Back skin control group (n=3 animals); [2] Back skin treated group (n=3 animals); [3] Tail skin control group (n=3 animals); and [4] Tail skin treated group (n=3 animals).

2014-02-25 | E-GEOD-55135 | biostudies-arrayexpress

Therapeutic effect of anti-KLK5 and KLK7 in a mouse model of atopic dermatitis

Project description:To investigate the effect of blocking the activity of KLK5 and KLK7 in the skin in a model of atopic dermatitis, we treated mice inhibitory antibodies against KLK5 and KLK7.

2023-03-01 | GSE205530 | GEO

Transcription profiling by array of lesional and non-lesional skin from atopic dermatitis patients and healthy individuals

Project description:Atopic dermatitis (AD) is a common inflammatory skin disease with a T(H)2 and T22 immune polarity. Despite recent data showing a genetic predisposition to epidermal barrier defects in some patients, a fundamental debate still exists regarding the role of barrier abnormalities versus immune responses in initiating the disease. An extensive study of nonlesional AD (ANL) skin is necessary to explore whether there is an intrinsic predisposition to barrier abnormalities, background immune activation, or both in patients with AD. We sought to characterize ANL skin by determining whether epidermal differentiation and immune abnormalities that characterize lesional AD (AL) skin are also reflected in ANL skin. We performed genomic and histologic profiling of both ANL and AL skin lesions (n = 12 each) compared with normal human skin (n = 10). We found that ANL skin is clearly distinct from normal skin with respect to terminal differentiation and some immune abnormalities and that it has a cutaneous expansion of T cells. We also showed that ANL skin has a variable immune phenotype, which is largely determined by disease extent and severity. Whereas broad terminal differentiation abnormalities were largely similar between involved and uninvolved AD skin, perhaps accounting for the background skin phenotype, increased expression of immune-related genes was among the most obvious differences between AL and ANL skin, potentially reflecting the clinical disease phenotype. Our study implies that systemic immune activation might play a role in alteration of the normal epidermal phenotype, as suggested by the high correlation in expression of immune genes in ANL skin with the disease severity index. Genomic profile of paired samples of ANL and AL skin lesions from 12 patients compared with normal human skin (n = 8). For some patients, only 1 sample was available.

2011-10-12 | E-GEOD-32924 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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