Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression analysis of epidermal barrier functions associated genes in mouse epidermis treated by All-trans retinoic acid and Nicotinamide

ABSTRACT: Investigation of molecular mechanisms of impaired skin barrier by ATRA in mouse epidermis

ORGANISM(S): Mus musculus

PROVIDER: GSE124181 | GEO | 2018/12/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression analysis of epidermal barrier functions associated genes in HaCaT cell treated by All-trans retinoic acid and Nicotinamide

Project description:Investigation of molecular mechanisms of impaired skin barrier by ATRA

2018-12-21 | GSE124179 | GEO

Expression analysis of epidermal barrier functions associated genes in mouse epidermis treated by All-trans retinoic acid and Nicotinamide

Project description:Expression analysis of epidermal barrier functions associated genes in mouse epidermis treated by All-trans retinoic acid and Nicotinamide

| PRJNA510954 | ENA

Expression analysis of epidermal barrier functions associated genes in HaCaT cell and mouse epidermis treated by All-trans retinoic acid and Nicotinamide

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-12-21 | GSE124183 | GEO

Expression analysis of epidermal barrier functions associated genes in HaCaT cell and mouse epidermis treated by All-trans retinoic acid and Nicotinamide

Project description:Expression analysis of epidermal barrier functions associated genes in HaCaT cell and mouse epidermis treated by All-trans retinoic acid and Nicotinamide

| PRJNA510955 | ENA

Evidence for the critical role of retinoid X receptor in rexinoid-induced increase in cellular all-trans-retinoic acid

Project description:Rexinoids are agonists of nuclear rexinoid X receptors (RXR) that heterodimerize with other nuclear receptors to regulate gene transcription. A number of selective RXR agonists have been developed for clinical use but their application has been hampered by the unwanted side effects associated with the use of rexinoids and a limited understanding of their mechanisms of action across different cell types. Previous studies from this laboratory showed that treatment of organotypic human epidermis with the low toxicity UAB30 and UAB110 rexinoids resulted in increased steady-state levels of all-trans-retinoic acid (ATRA), the obligatory ligand of the RXR-RAR heterodimers. Here, we investigated the molecular mechanism underlying the increase in ATRA levels using a dominant negative RXRα that lacks the activation function 2 (AF-2) domain. The results demonstrated that overexpression of dnRXRα in human organotypic epidermis markedly reduced signaling by resident ATRA, suggesting the existence of endogenous RXR ligand, diminished the biological effects of UAB30 and UAB110 on epidermis morphology and gene expression, and nearly abolished the rexinoid-induced increase in ATRA levels. Global transcriptome analysis of dnRXRα-rafts in comparison to empty vector-transduced rafts showed that over 95% of the differentially expressed genes in rexinoid-treated rafts constitute direct or indirect ATRA-regulated genes. Thus, the biological effects of UAB30 and UAB110 are mediated through the AF-2 domain of RXRα with minimal side effects in human epidermis. As ATRA levels are known to be reduced in certain epithelial pathologies, treatment with UAB30 and UAB110 may represent a promising therapy for normalizing the endogenous ATRA concentration and signaling in epithelial tissues.

2024-04-02 | GSE244387 | GEO

Expression analysis of epidermal barrier functions associated genes in HaCaT cell treated by All-trans retinoic acid and Nicotinamide

Project description:Expression analysis of epidermal barrier functions associated genes in HaCaT cell treated by All-trans retinoic acid and Nicotinamide

| PRJNA510952 | ENA

Clinical Trial of All-trans-retinoic Acid, Bevacizumab and Atezolizumab in Colorectal Cancer

Project description:The main purpose of this clinical trial is to learn about the good and the bad effects of all trans retinoic acid (ATRA), atezolizumab and bevacizumab as a possible treatment for advanced colorectal patients. Participants will be treated with the following combination of these drugs: 1. ATRA will be given in a pill form to be taken twice a day at home for 7 days starting on day 1 of a cycle. 2. Atezolizumab will be given through a vein in arm or through mediport over 60-90 minutes every 2 weeks in the outpatient chemotherapy infusion centers at UTSW. 3. Bevacizumab will be given through a vein in arm or through mediport over 20-40 minutes every 2 weeks in the outpatient chemotherapy infusion centers at UTSW.

| 70824 | ecrin-mdr-crc

Grhl3 is essential for epidermal barrier repair from both physical and immune injury, relevance to lesional skin disease

Project description:Epidermal barrier repair mechanisms activated in psoriasis lesions are likely involved in limiting the severity of this disease. We show that loss of grainyhead-like 3 (Grhl3), a pro-terminal differentiation factor in the epidermis, is sufficient to trigger greater sensitivity to and delayed resolution of epidermal lesions resulting from either physical or immune mediated barrier injury. After stimulation of Toll like receptors, the loss of Grhl3 resulted in increased epidermal damage with a striking increase in basal cell proliferation, hyperplasia of partially differentiated suprabasal layers, and a transcriptional profile highlighted by the overexpression of epidermal wound response and alarmin genes. This study reveals an important role for the epidermis in the initiation and recovery from immune-mediated lesions, and indicated that the epidermal regulator Grhl3 acts to both suppress disease initiation and resolve existing lesions. This work suggests that treatments focused on improving barrier function could be used preventatively and therapeutically in psoriasis. Whole skin was collected from E16.5 mouse backskins for Grhl3 ChIP. Adult epidermis for depilation and imiquimod experiments was seperated from dermis using dispase prior to Grhl3 ChIP.

2014-09-01 | E-GEOD-52648 | biostudies-arrayexpress

All?trans retinoic acid alters the expression of the tight junction proteins Claudin?1 and ?4 and epidermal barrier function?associated genes in the epidermis.

Project description: Not available

| S-EPMC6414175 | biostudies-literature

Analysis of chromatin accessibility in human epidermis identifies putative barrier dysfunction-sensing enhancers

Project description:To identify putative gene regulatory regions that respond to epidermal injury, we mapped chromatin dynamics in a stratified human epidermis during barrier maturation and disruption. Engineered skin substitutes (ESS) cultured at the air-liquid interface were used as a model of developing human epidermis with incomplete barrier formation. The epidermal barrier stabilized following engraftment onto immunocompromised mice, and was compromised again upon injury. Modified formaldehyde-assisted isolation of regulatory elements (FAIRE) was used to identify accessible genomic regions characteristic of monolayer keratinocytes, ESS in vitro, grafted ESS, and tape-stripped ESS graft. We mapped differentiation- and maturation-associated changes in transcription factor binding sites enriched at each stage and observed overrepresentation of AP-1 gene family motifs in barrier- deficient samples. Transcription of TSLP, an important effector of immunological memory in response to allergen exposure, was dramatically elevated in our barrier-deficient samples. We identified dynamic DNA elements that correlated with TSLP induction and may contain enhancers that regulate TSLP. Two dynamic regions were located near the TSLP promoter and overlapped with allergy-associated SNPs rs17551370 and rs2289877, strongly implicating these loci in the regulation of TSLP expression in allergic disease. Additional dynamic chromatin regions ~250kb upstream of the TSLP promoter were found to be in high linkage disequilibrium with allergic disease SNPs. Taken together, these results define dynamic chromatin accessibility changes during epidermal development and dysfunction.

2017-08-28 | GSE101835 | GEO

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