title: Tenascin-C is upregulated in the skin lesions of patients with atopic dermatitis.
abstract: BACKGROUND
  Tenascin-C is a large, hexameric extracellular matrix glycoprotein that is expressed during embryogenesis, carcinogenesis and wound healing. In normal adult human skin the expression level of tenascin-C is low, but levels are elevated in skin tumors and rise significantly in the dermal compartment during wound healing. 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 role in AD.
  
  
  METHODS
  We screened for differentially 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 moderately 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.
  
  
  CONCLUSIONS
  These results suggest that upregulation of the tenascin-C expression is specific to AD lesions, and that tenascin-C may therefore play a critical role in regulating the underlining inflammatory processes, which are involved in the pathology of AD.
authors.affiliation: Genox Research Inc., Ibaraki, Laboratory of Seeds Finding Technology, Eisai Co. Ltd., 5-1-3 Tokodai, Tsukuba-shi, Ibaraki 300-2635, Japan. k6-ogawa@hhc.eisai.co.jp
authors.forename: Kaoru
authors.initials: K
authors.lastname: Ogawa
authors.forename: Mikito
authors.initials: M
authors.lastname: Ito
authors.forename: Kaori
authors.initials: K
authors.lastname: Takeuchi
authors.forename: Akiko
authors.initials: A
authors.lastname: Nakada
authors.forename: Masayuki
authors.initials: M
authors.lastname: Heishi
authors.forename: Hajime
authors.initials: H
authors.lastname: Suto
authors.forename: Kouichi
authors.initials: K
authors.lastname: Mitsuishi
authors.forename: Yuji
authors.initials: Y
authors.lastname: Sugita
authors.forename: Hideoki
authors.initials: H
authors.lastname: Ogawa
authors.forename: Chisei
authors.initials: C
authors.lastname: Ra
mesh_terms: D000818:Animals; D003876:Dermatitis, Atopic / Q000378:metabolism*; D005786:Gene Expression Regulation; D006801:Humans; D007371:Interferon-gamma / Q000502:physiology; D018793:Interleukin-13 / Q000502:physiology; D015847:Interleukin-4 / Q000502:physiology; D015603:Keratinocytes / Q000378:metabolism; D008297:Male; D051379:Mice; D011565:Psoriasis / Q000378:metabolism; D012867:Skin / Q000378:metabolism*; D019063:Tenascin / Q000235:genetics*; D015854:Up-Regulation
chemical_list: D018793:Interleukin-13; D019063:Tenascin; D015847:Interleukin-4; D007371:Interferon-gamma