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Expression data from normal human epidermal keratinocytes undergoing density-induced differentiation and treated with EGF

ABSTRACT: Combining genome-wide microarray and functional analyses, we found that EGFR activation abrogates barrier function, increasing transepidermal water loss (TEWL) and transepithelial permeability of water-soluble ions and higher molecular weight dextrans, in part by disrupting the expression of tight junction proteins. EGF decreases certain lipid matrix free fatty acids and ceramides by its actions to repress the expression of specific biosynthetic enzymes. Activation of EGFR inhibits cornified envelope formation by regulating the expression of 59 percent of the known contributing genes. EGF-responsiveness enriches more than 100 genes known to be associated with skin diseases. These data are used to obtain 2,676 density-dependent genes that are differentially expressed in response to EGF treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE32217 | GEO | 2012/05/03

SECONDARY ACCESSION(S): PRJNA147227

REPOSITORIES: GEO

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Expression data from normal human epidermal keratinocytes undergoing density-induced differentiation and treated with EGF

Project description:Combining genome-wide microarray and functional analyses, we found that EGFR activation abrogates barrier function, increasing transepidermal water loss (TEWL) and transepithelial permeability of water-soluble ions and higher molecular weight dextrans, in part by disrupting the expression of tight junction proteins. EGF decreases certain lipid matrix free fatty acids and ceramides by its actions to repress the expression of specific biosynthetic enzymes. Activation of EGFR inhibits cornified envelope formation by regulating the expression of 59 percent of the known contributing genes. EGF-responsiveness enriches more than 100 genes known to be associated with skin diseases. These data are used to obtain 2,676 density-dependent genes that are differentially expressed in response to EGF treatment. The 16 microarrays were preprocessed using the 5th percentile of region method in dChip. Genes with at least a 1.5 fold difference between the untrated samples at 50% and 100% confluent cell density were exported for further analysis. Two-way ANOVA was used to identify differentially expressed genes by either density or treatment factors using JMP Genomics 4.1 (SAS). Multiple hypothesis testing was corrected by Benjamini-Hochberg false discovery rate control at the 0.05 level. Pair-wise comparisons were performed using the TukeyM-bM-^@M-^Ys Honestly Significant Difference test.

2012-05-02 | E-GEOD-32217 | biostudies-arrayexpress

Serpinb3a contributes to early skin inflammation following allergen exposure

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Epidermal RORα maintains barrier integrity and prevents allergic inflammation by regulating late differentiation and lipid metabolism

Project description:The skin epidermis provides a vital barrier for preventing transepidermal water loss (TEWL) and environmental stimuli. However, the molecular mechanisms ensuring barrier integrity remain not fully understood. RORα is a nuclear receptor highly expressed in the epidermis of normal skin. However, its epidermal expression is significantly reduced in the lesions of multiple inflammatory skin diseases. In this study, using mice with epidermis-specific Rora gene deletion (RoraEKO), we have demonstrated the central roles of RORα in stabilizing skin barrier function. Albeit the lack of spontaneous skin lesion or dermatitis, RoraEKO mice exhibited elevated TEWL rate and skin features indicating barrier dysfunction. The histological and lipidomic analysis uncovered low levels of cornified envelope proteins and aberrant ceramide composition in the RoraEKO epidermis, implying disturbed late epidermal differentiation. In parallel, RNA-seq analysis revealed altered transcription levels of gene clusters related to “keratinization” and “lipid metabolism” in RORα deficient epidermis. Importantly, epidermal Rora ablation greatly amplified percutaneous allergic inflammatory responses to oxazolone in a mouse allergic contact dermatitis (ACD) model. Our results substantiated the essence of epidermal RORα in maintaining late keratinocyte differentiation and normal barrier function while suppressing cutaneous inflammation.

2024-10-23 | GSE275323 | GEO

6KR-EGFR expressing MCF7 following EGF or HRG stimulation

Project description:EGF and HRG, growth factor ligands for EGFR and ErbB3/4 receptor, induce transient and sustained ERK activity associated with cellular proliferation and differentiation of MCF-7 cells, respectively. To rigorously analyze the effect of ERK signal duration for mRNA expression dynamics and its relationship with cell determination, we modified the EGF-triggered ERK signal duration by changing the EGFR activation dynamics by impairing the ubiquitination and degradation process. Mutation of the six lysine residues (6KR; K692, K713, K730, K843, K905 and K946) of the EGFR responsible for ubiquitin conjugation has shown sustained phosphorylation of the receptor (Huang et al, 2006; Goh et al, 2010). Therefore we constructed the MCF-7 cell lines that stably express 6KR EGFR (6KR), and analyzed signaling and mRNA expression dynamics in response to EGF and HRG.

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Serpinb3a contributes to early skin inflammation following allergen exposure

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Glucosylceramide fed mice skin before SDS treatment (0d), after SDS treatment (2d)

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2012-03-31 | E-GEOD-28086 | biostudies-arrayexpress

H1299 EGF and Iressa stimulation

Project description:Controlled activation of epidermal growth factor receptor (EGFR) is systematically guaranteed at the molecular level, however aberrant activation of EGFR is frequently found in cancer. Transcription induced by EGFR activation often involves coordinated expression of genes that positively and negatively regulate the original signaling pathway, therefore alterations in EGFR kinase activity may reflect changes in gene expression associated with the pathway. In this study, we investigated transcriptional changes following EGF stimulation with or without the EGFR kinase inhibitor Iressa in H1299 human non-small-cell lung cancer cells (parental H1299, H1299 cells which overexpress wild-type: EGFR-WT and mutant EGFR: L858R). Our results clearly showed differences in transcriptional activity in the absence or presence of EGFR kinase activity, and genes sharing the same molecular functions showed distinct expression dynamics. The results showed particular enrichment of EGFR/ErbB signaling-related genes in a differentially expressed gene set, and significant protein expression of MIG6/RALT(ERRFI1), an EGFR negative regulator, was confirmed in L858R. High MIG6 protein expression was correlated with basal EGFR phosphorylation and inversely correlated with EGF-induced ERK phosphorylation levels. Investigation of NCI-60 cell lines showed that ERRFI1 expression was correlated with EGFR expression regardless of tissue type. These results suggest that cells accumulate MIG6 as an inherent negative regulator to suppress excess EGFR activity when basal EGFR kinase activity is considerably high. Taken together, an EGFR mutation can cause transcriptional changes to accommodate the activation potency of the original signaling pathway at the cellular level.

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Glucosylceramide fed mice skin before SDS treatment (0d), after SDS treatment (2d)

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Expression data from HELA cells subject to EGF stimulation

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Transcription profiling of rat astrocytes treated with epidermal growth factor (EGF)

Project description:Primary cultures of astrocytes from rat optic nerve heads were treated with EGFR ligand, EGF. Two cell lines from two different rat donors were used. The sister cell cultures were set as control and EGF treated groups. Experiment Overall Design: experiment #1: compared control astrocyte cultures to sister cultures treated with EGF for 4 hours. Experiment Overall Design: experiment #2: compared control astrocyte cultures to sister cultures treated with EGF for 12 hours

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