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Identification of genes differentially expressed in atopic dermatitis, contact dermatitis, and psoriasis by microarray analyses

Identification of genes differentially expressed in atopic dermatitis, contact dermatitis, and psoriasis by microarray analyses 1

Identification of genes differentially expressed in atopic dermatitis, contact dermatitis, and psoriasis by microarray analyses. Confirmation of protein expression profiles in atopic and contact dermatitis, and psoriasis by immunohistochemical analyses. Atopic dermatitis (AD; eczema) is characterized by a widespread abnormality in cutaneous barrier function and propensity to inflammation. However, microarray analysis is intrinsically restricted by preselection of genes represented on an array and by annotations from which gene expression is quantified. Comparative transcriptomic analyses of atopic dermatitis and psoriasis reveal shared neutrophilic inflammation. We conducted gene expression microarray analyses to identify distinct and commonly dysregulated expression in AD (based on Hanifin and Rajka criteria) and psoriatic lesions.

Psoriasis is a chronic inflammatory skin disease characterized by the formation of scaly and erythematous plaques 2Whole genome expression analysis revealed alterations in numerous pathways related to metabolism and proliferation in non-involved skin of psoriasis patients as compared to non-psoriatic individuals, indicating that even in clinically non-involved skin of psoriasis patients molecular events opposing contact dermatitis may occur. Psoriasis and allergic contact dermatitis (ACD) are highly prevalent, complex inflammatory skin diseases characterized by a combination of epithelial alterations and deviated T cell immunity 1, 2. Significant differentially expressed genes were defined with a significance threshold of corrected p-values. In the constellation of genes differentially expressed in AE skin compared to healthy control skin, we have identified several potential susceptibility genes that may play a critical role in the pathological condition of AE. Omics technologies including proteomics (11) and microarrays (12) are powerful tools to identify the underlying molecular mechanisms of disease and potential biomarkers. Park et al identified 31 atopic dermatitis-related candidate proteins from a proteomic analysis (13). For instance, the study by Nomura et al (15), used DNA microarray analysis to compare the complex gene expression pattern of skin lesions from AD and psoriasis. Raw data were normalized prior to differential expression analysis (Fig.

We identified differentially expressed genes (DEGs) with altered expression in psoriasis lesions (n 216 patients), as well as candidate genes near susceptibility loci from psoriasis GWAS studies. Results:Transcriptome analysis using skin lesion, CD4+ T cells, monocytes and eosinophils derived from AE patients identified some differentially expressed genes which became biologically relevant in the following studies. In this study, we performed global gene expression analysis of skin from DM patients and healthy controls. 05), we identified 946 unique genes that were differentially regulated at least 2-fold in DM skin relative to healthy skin: we term this the DM gene module (Table S2). Across patient samples, there was a good correlation between microarray and QRT-PCR values for each of the four genes (Spearman 0.

Plos One: Allergic Contact Dermatitis In Psoriasis Patients: Typical, Delayed, And Non-interacting

Our analysis combines microarray data from three separate studies, each of which profiled gene expression using the same oligonucleotide array platform 8, 11, 19. Using these data, we identify genes differentially expressed between PP and PN skin (i. To address this question, we evaluated each DEG individually, and assigned each DEG to a cell type if the gene was specifically expressed in that cell type (FDR 0. Bernard FX, Morel F, Camus M, Pedretti N, Barrault C, Garnier J, Lecron JC: Keratinocytes under fire of proinflammatory cytokines: bona fide innate immune cells involved in the physiopathology of chronic atopic dermatitis and psoriasis. This altered expression of Blimp-1 in human eczematous skin prompted us to examine the physiological role of Blimp-1 in adult mouse keratinocytes. (LN) At 2 mo after 4OHT injection, Ctrl and CKO mice were used for contact hypersensitivity tests. Microarray analyses revealed 93 up-regulated genes and 109 down-regulated genes that were altered by more than twofold in the mice with deleted Prdm1 (Tables S1 and S2). This analysis clearly differentiated involved psoriatic skin from uninvolved and normal skin. Ten of the 177 genes were also differentially expressed in uninvolved skin, and several mapped to regions previously shown to harbor psoriasis susceptibility loci. Some PS susceptibility loci coincide with loci identified in genome-wide scans of other autoimmune/inflammatory diseases including chromosomes 1q21 atopic dermatitis (AD) (21), 3q21 rheumatoid arthritis (RA) and AD (22,23), 14q31 Grave’s disease (GD), insulin dependent diabetes mellitus (IDDM) (24,25), 16p irritable bowel disease (IBD) (26) and 17q24.

Cellular Dissection Of Psoriasis For Transcriptome Analyses And The Post-gwas Era