イタノ ナオキ   ITANO NAOKI
  板野 直樹
   所属   京都産業大学  生命科学部 先端生命科学科
   職種   教授
言語種別 英語
発行・発表の年月 2012/01
形態種別 研究論文
査読 査読あり
標題 Enhanced Inflammation and Accelerated Wound Closure Following Tetraphorbol Ester Application or Full-Thickness Wounding in Mice Lacking Hyaluronan Synthases Has1 and Has3
執筆形態 その他
掲載誌名 JOURNAL OF INVESTIGATIVE DERMATOLOGY
出版社・発行元 NATURE PUBLISHING GROUP
巻・号・頁 132(1),pp.198-207
著者・共著者 Judith A. Mack,Ron J. Feldman,Naoki Itano,Koji Kimata,Mark Lauer,Vincent C. Hascall,Edward V. Maytin
概要 Hyaluronan (HA) is an abundant matrix molecule, the function of which in the skin remains to be fully defined. To explore the roles of HA in cutaneous injury responses, double-knockout mice (abbreviated as Has1/3 null) that lack two HA synthase enzymes (Has1 and Has3), but still express functional Has2, were used in two types of experiments: (i) application of 12-O-tetradecanoylphorbol-13-acetate (TPA) and (ii) full-thickness wounding of the skin. Uninjured Has1/3-null mice were phenotypically normal. However, after TPA, the accumulation of HA that normally occurs in wild-type epidermis was blunted in Has1/3-null epidermis. In excisional wound-healing experiments, wound closure was significantly faster in Has1/3 null than in wild-type mice. Coincident with this abnormal wound healing, a marked decrease in epidermal and dermal HA and a marked increase in neutrophil efflux from cutaneous blood vessels were observed in Has1/3-null skin relative to wild-type skin. Has1/3-null wounds displayed an earlier onset of myofibroblast differentiation. In summary, selective loss of Has1 and Has3 leads to a proinflammatory milieu that favors recruitment of neutrophils and other inflammation-related changes in the dermis.
DOI 10.1038/jid.2011.248
ISSN 0022-202X