Tenascin-C is upregulated in the skin lesions of patients with atopic dermatitis

被引:24
作者
Ogawa, K
Ito, M
Takeuchi, K
Nakada, A
Heishi, M
Suto, H
Mitsuishi, K
Sugita, Y
Ogawa, H
Ra, C
机构
[1] Genox Res Inc, Ibaraki 3002635, Japan
[2] Eisai & Co Ltd, Lab Seeds FInding Technol, Tsukuba, Ibaraki 3002635, Japan
[3] Juntendo Univ, Sch Med, Atopy Allergy Res Ctr, Tokyo 113, Japan
[4] Juntendo Univ, Sch Med, Dept Dermatol, Tokyo 113, Japan
[5] Nihon Univ, Grad Sch Med Sci, Adv Med Res Ctr, Div Mol Cell Immunol & Allergol, Tokyo, Japan
关键词
atopic dermatitis; extracellular matrix; real-time RT-PCR; keratinocyte; NC/Nga mice;
D O I
10.1016/j.jdermsci.2005.06.001
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 [皮肤病与性病学];
摘要
Background: Tenascin-C is a large, hexameric extracellular matrix glycoprotein that is expressed during embryogenesis, carcinogenesis and wound heating. In normal adult human skin the expression level of tenascin-C is tow, but levels are elevated in skin tumors and rise significantly in the dermal compartment during wound heating. Although the expression of tenascin-C could be upregulated by inflammatory cytokines, the role of tenascin-C in atopic dermatitis (AD) is still unclear. Objective: To identify genes that plays a rote in AD. Methods: We screened for differentialty expressed genes in lesional. and non-lesional skin of AD patients using DNA microarray. Then we monitored with quantitative PCR the expression of the novel disease related genes in human keratinocytes or pinnae from NC/Nga mice. Results: We found that tenascin-C gene expression was expressed at higher levels in lesional skin compared to non-lesional skin of the patients, whereas it was not upregulated in the skin of psoriatic patients or healthy controls. In human cultured keratinocytes, tenascin-C was markedly upregulated by IL-4 and IL-13, and moderatety upregulated by IFN-gamma. Tenascin-C expression was also upregulated in the AD-like skin lesions induced in NC/Nga mice ears by intradermal injection of mite antigen, and this upregulation was inhibited by prednisolone. Conclusion: These results suggest that upregulation of the tenascin-C expression is specific to AD lesions, and that tenascin-C may therefore play a critical rote in
引用
收藏
页码:35 / 41
页数:7
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