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

ABSTRACT: Dietary glucosylceramide (GC) improves skin barrier function. To elucidate the molecular mechanisms involved, we used a microarray system to analyze mRNA expression in SDS-treated dorsal skin of hairless mouse. Transepidermal water loss of mouse skin was increased by SDS treatment and the increase was significantly reduced by prior oral administration of glucosylceramides. Microarray-evaluated mRNA expression ratios showed statistically significant increase of expression of genes related to cornified envelope and tight junction formation versus all genes in glucosylceramide-fed/SDS-treated mouse skin. We then examined the contribution of glucosylceramide metabolites to tight junction formation of cultured keratinocytes. SDS treatment of cultured keratinocytes significantly decreased the transepidermal electrical resistance, and the decrease was significantly ameliorated in the presence of sphingosine or phytosphingosine, the major metabolites of glucosylceramide. These results suggest that oral administration of glucosylceramide improves skin barrier function by upregulating genes associated with both cornified envelope and tight junction formation. Two-condition experiment, effect of oral intake of GC on mice skin before SDS treatment (0d), and after SDS treatment(2d), Biological replicates: 3 replicates for 0d, 4 replicates for 2d.

ORGANISM(S): Mus musculus

SUBMITTER: Ritsuro Ideta

PROVIDER: E-GEOD-28086 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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

Project description:Dietary glucosylceramide (GC) improves skin barrier function. To elucidate the molecular mechanisms involved, we used a microarray system to analyze mRNA expression in SDS-treated dorsal skin of hairless mouse. Transepidermal water loss of mouse skin was increased by SDS treatment and the increase was significantly reduced by prior oral administration of glucosylceramides. Microarray-evaluated mRNA expression ratios showed statistically significant increase of expression of genes related to cornified envelope and tight junction formation versus all genes in glucosylceramide-fed/SDS-treated mouse skin. We then examined the contribution of glucosylceramide metabolites to tight junction formation of cultured keratinocytes. SDS treatment of cultured keratinocytes significantly decreased the transepidermal electrical resistance, and the decrease was significantly ameliorated in the presence of sphingosine or phytosphingosine, the major metabolites of glucosylceramide. These results suggest that oral administration of glucosylceramide improves skin barrier function by upregulating genes associated with both cornified envelope and tight junction formation.

2012-04-01 | GSE28086 | GEO

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

2012-05-03 | GSE32217 | GEO

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

Early-onset pediatric atopic dermatitis is characterized by Th2/Th17/Th22- centered inflammation and lipid alterations

Project description:Background: While atopic dermatitis (AD) often starts in early childhood, detailed tissue profiling of early-onset AD in children is lacking, hindering therapeutic development for this patient population with a particularly high unmet need of better treatments. Objective: We sought to globally profile the skin of infants with AD compared to adults with AD and healthy controls. Methods: We performed microarray, RT-PCR and fluorescence microscopy studies in infants and young children (<5yo) with early-onset AD (<6mo) compared to age-matched controls and adults with longstanding AD. Results: Transcriptomic analyses revealed profound differences between early-onset pediatric vs. longstanding adult AD, not only in lesional but also non-lesional tissues. While both patient populations harbored Th2-centered inflammation, pediatric AD also showed significant Th17-skewing, but lacked the Th1 upregulation that characterizes adult AD. Defects in lipid barrier (e.g. ELOVL3, DGAT2) and tight junction regulation (e.g. Claudins 8 and 23) were evident in both groups but, unlike adult AD which showed the classic downregulation of epidermal differentiation and cornification products, pediatric AD exhibited relatively normal expression of these genes. Some lipid-associated mediators (such as FAR2 and FA2H) even showed preferential downregulation in pediatric AD, and lipid barrier genes (FA2H, DGAT2) showed inverse correlations with transepidermal water loss/TEWL, a functional measure of the epidermal barrier. Conclusions: Children and adult AD skin samples share lipid metabolism and tight junction alterations, but epidermal differentiation complex defects are only present in adult AD, potentially resulting from chronic immune aberration that is not yet present in early-onset disease.

2018-05-21 | GSE107361 | GEO

Repeated social defeat stress (R-SDS)-induced changes in gene expression profiles in the medial prefrontal cortex (mPFC)

Project description:To identify R-SDS-induced changes in gene expression profiles in the mPFC, we performed transcriptome analysis in the mPFC without or with R-SDS. We separately analyzed the data from susceptible mice, which showed social avoidance after R-SDS, and resilient mice, which did not, in addition to those from naïve mice.

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Transcription profiling of Enterococcus faecalis V583 treated with SDS and bovine bile

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2007-08-01 | E-TABM-242 | biostudies-arrayexpress

The effect of engineered del(7q) on induced pluripotent stem cells (iPSCs) derived from patients with Shwachman Diamond Syndrome (SDS).

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2019-07-26 | GSE118372 | GEO

Transcriptome analysis of microglia isolated from the mPFC or NAc without or with repeated social defeat stress (R-SDS)

Project description:To identify R-SDS-induced changes in gene expression profiles in medial prefrontal cortex (mPFC) and nucleus accumbens (NAc) microglia, we performed transcriptome analysis in mPFC and NAc microglia without or with R-SDS. Based on our observation that TLR2/TLR4 mediate R-SDS-induced activation of mPFC microglia, we performed the analysis in wild-type (WT) mice and TLR2/TLR4-double knockout (TLR-DKO) mice.

2018-08-09 | GSE115995 | GEO

RNA-Seq of U251 glioblastoma cell line with and without (-)-SDS-1-021.

Project description:RNA-Seq analyses polysome-bound mRNAs of glioblastoma cell line NSC11 after 10nM (-)-SDS-1-021 treatement to evaluate drug-induced changes in mRNA translation

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Sigma factor B (sigB) response to stress conditions (0.05% SDS and 5mM Diamide)

Project description:The numerous sigma factors present in Mycobacterium tuberculosis (MTB) are indicative of adaptability to different environmental conditions. In this report we describe the sigma factor B (sigB) regulon and the phenotypes of a MTB sigB mutant strain exposed to different stresses like SDS and Diamide. This experiment set compares expression profiles between H37Rv wild type and H37Rv sigB null mutant as well as under different stress conditions. Both H37Rv wild type and H37Rv sigB null mutants were treated with either 0.05% SDS or 5mM Diamide for 60 min and their expression profiles were compared with untreated wild type or mutant controls.

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