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Towards profiling the gene expression of fibroblasts from atopic dermatitis patients: human 8K complementary DNA microarray
Author(s) -
Park Y.D.,
Lyou Y.J.,
Lee K.J.,
Lee D.Y.,
Yang J.M.
Publication year - 2006
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.2006.02480.x
Subject(s) - gene expression profiling , microarray , atopic dermatitis , candidate gene , gene expression , gene , biology , microarray analysis techniques , pathogenesis , dna microarray , gene chip analysis , complementary dna , microbiology and biotechnology , immunology , genetics
Summary Background High‐throughput technologies, including DNA‐chip array, have been used to search for the genes that are dysregulated in human diseases. The atopic dermatitis (AD)‐associated genes are gradually being reported; however, the differentially altered gene expression profiles of atopic fibroblasts have not been well elucidated. Objective We wanted to gain more insights into AD and to find candidate genes, especially in regards to the role of fibroblasts in the pathogenesis of AD. Methods cDNA microarray (8K) profiling of the primary cultured AD patients‐derived fibroblasts was conducted by a pooling method of the recruited 22 normal controls, the 10 extrinsic type (ADe) patients and the 10 intrinsic type (ADi) patients. SAM analysis of the microarray results (2‐fold cut‐off) was conducted to select the candidate genes. Quantification by real‐time PCRs confirmed the array data in the randomized paired samples (normal vs. ADe n =10; normal vs. ADi n =10). Results We listed the 22 up‐regulated and 95 down‐regulated genes in the AD fibroblasts. Real‐time PCR results showed that several genes such as hyaluronan synthase 2 (HAS2), TNF‐α‐induced protein 6 (TNFAIP6) and IL‐8 were matched with the array results with statistical significance. Conclusion These results suggest gene expression profiles that are associated with AD and this implied that fibroblasts may play important roles in the AD pathogenesis. We provided new insights into three candidate genes such as HAS2, TNFAIP6 and IL‐8 with respect to their involvement in AD disease.