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KMID : 0984920150170020116
Journal of Skin Barrier Research
2015 Volume.17 No. 2 p.116 ~ p.116
Transcriptome Changes for Psoriasis Vulgaris and Atopic Dermatitis in Skin Barrier Homeostasis
Jung Min-Young

Nam Chan-Hee
Park Byung-Cheol
Kim Myung-Hwa
Hong Seung-Phil
Abstract
Atopic dermatitis (AD) and psoriasis vulgaris (PSO) are most representative inflammatory skin disease. Skin barrier dysfunction is commonly seen in AD and PSO. However, their clinical features are quite different due to the pathogenetic difference. To deeply understand the clinical as well as pathogenetic differences, we have analyzed the genes involved in the epidermal lipid synthesis, epidermal development process and immune responses in the skin of AD and PSO patients. We have compared the transcriptomes of lesional skin from 6 adults AD patients (males), 4 PSO patients (1 female and 3 males) and 6 healthy young volunteers (19~24 years of age, 3 females and 3 males) by high-throughput complementary DNA sequencing (RNA-seq). For the gene expression estimation, Cufflinks v2.1.1 was used that is the gene annotation database of Ensembl release 72. 3,121 and 6,669 differentially expressed genes (DEGs) were identified in the skin of AD and PSO patients, respectively, compared with healthy skin (p<0.05). Comparing two disease groups, an overlap containing 397 genes was detected. The criterion for inclusion in the list was at least two-fold under- or over- expression in the same direction in both diseases. These transcriptomes contained AD- and PSO-associated genes for confirming diseases such as carbonic anhydrase ¥± (CA¥±), neural epidermal growth factor ¥± (NELL¥±), thymus and activation-regulated chemokine (TARC/CCL17), ¥â-defensin-2 (DEFB4), psoriasin (S100A7), elafin (PI3), IL-17A, Ki67, and IL-12. The DEGs of AD and PSO groups were clustered into the GOs related to lipids metabolism, epidermal differentiation and development process, and immune response. This data help us understand the gene expressional differences in the skin barrier homeostasis pathway, cytoskeletal changes, and inflammatory response.
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