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 2006/07
形態種別 研究論文
査読 査読あり
標題 SHAP potentiates the CD44-mediated leukocyte adhesion to the hyaluronan substratum
執筆形態 その他
掲載誌名 JOURNAL OF BIOLOGICAL CHEMISTRY
出版社・発行元 AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
巻・号・頁 281(29),pp.20303-20314
著者・共著者 Lisheng Zhuo,Akiko Kanamori,Reiji Kannagi,Naoki Itano,Jiwen Wu,Michinari Hamaguchi,Naoki Ishiguro,Koji Kimata
概要 CD44-hyaluronan (HA) interaction is involved in diverse physiological and pathological processes. Regulation of interacting avidity is well studied on CD44 but rarely on HA. We discovered a unique covalent modification of HA with a protein, SHAP, that corresponds to the heavy chains of inter-alpha-trypsin inhibitor family molecules circulating in blood. Formation of the SHAP(.)HA complex is often associated with inflammation, a well known process involving the CD44-HA interaction. We therefore examined the effect of SHAP on the CD44-HA interaction-mediated lymphocyte adhesion. Under both static and flowing conditions, Hut78 cells (CD44-positive) and CD44-transfected Jurkat cells (originally CD44-negative) adhered preferentially to the immobilized SHAP(.)HA complex than to HA. The enhanced adhesion is exclusively mediated by the CD44-HA interaction, because it was inhibited by HA, but not I alpha I, and was completely abolished by pretreating the cells with anti-CD44 antibodies. SHAP appears to potentiate the interaction by increasing the avidity of HA to CD44 and altering their distribution on cell surfaces. Large amounts of the SHAP(.)HA complex accumulate in the hyperplastic synovium of rheumatoid arthritis patients. Leukocytes infiltrated to the synovium were strongly positive for HA, SHAP, and CD44 on their surfaces, suggesting a role for the adhesion-enhancing effect of SHAP in pathogenesis.
DOI 10.1074/jbc.M506703200
ISSN 0021-9258