Role of Galectin-3 in Human Pulmonary Fibrosis

この論文にアクセスする

この論文をさがす

著者

    • NISHI Yumiko
    • Department of Internal Medicine, Toho University Sakura Medical Center
    • SANO Hideki
    • Department of Internal Medicine, Toho University Sakura Medical Center
    • OKADA Tomoaki
    • Department of Internal Medicine, Toho University Sakura Medical Center
    • KIKKAWA Kyoko
    • Department of Internal Medicine, Toho University Sakura Medical Center
    • TANABE Masaaki
    • Department of Internal Medicine, Toho University Sakura Medical Center
    • GOTO Tsukane
    • Department of Internal Medicine, Toho University Sakura Medical Center
    • MATSUZAWA Yasuo
    • Department of Internal Medicine, Toho University Sakura Medical Center
    • TOMIOKA Hisao
    • Department of Internal Medicine, Toho University Sakura Medical Center
    • LIU Fu-Tong
    • Department of Dermatology, University of California, Davis, School of Medicine
    • SHIRAI Koji
    • Department of Internal Medicine, Toho University Sakura Medical Center

抄録

<b>Background:</b> Galectin-3 is a β-galactoside-binding protein which is implicated in diverse physiological and pathological processes including human liver cirrhosis and a mouse lung fibrosis model. The aim of this study is to determine whether galectin-3 is involved in human lung fibrosis.<br> <b>Methods:</b> We measured galectin-3 concentration in bronchoalveolar lavage fluid (BALF) and examined its expression in alveolar macrophages from patients with interstitial lung disorders using ELISA and immunohistochemical staining, respectively. Using monocyte/macrophage cell lines <i>in vitro</i>, we examined the effect of cytokines on galectin-3 expression, and the opposite similarly by RT-PCR and Western blotting. Finally, we performed Micro Boyden chamber assay and Sircoll assay to determine whether galectin-3 induces migration and collagen synthesis, respectively, in fibroblasts.<br> <b>Results:</b> Galectin-3 was specifically increased in BALF from patients with idiopathic pulmonary fibrosis (IPF) and interstitial pneumonia associated with collagen vascular disease (CVD-IP). Galectin-3 levels in BALF seemed to be lower in IPF and CVD-IP patients receiving corticosteroid therapy. Alveolar macrophages from IPF patients expressed more galectin-3 compared with those from control. Galectin-3 expression was induced by tumor necrosis factor-alpha (TNF-α) and interferon (IFN)-γ in a monocytic cell line U937. Galectin-3 also induced mRNA expression and protein production of TNF-α and interleukin (IL)-8 in a macrophage cell line THP-1. This lectin stimulated NIH-3T3 fibroblast to induce migration and collagen synthesis <i>in vitro</i>.<br> <b>Conclusions:</b> These results suggest that galectin-3 is involved in the pathogenesis of human IPF and CVD-IP by activating macrophages and fibroblasts.<br>

収録刊行物

  • Allergology international : official journal of the Japanese Society of Allergology  

    Allergology international : official journal of the Japanese Society of Allergology 56(1), 57-65, 2007-03-01 

    Japanese Society of Allergology

参考文献:  49件

参考文献を見るにはログインが必要です。ユーザIDをお持ちでない方は新規登録してください。

被引用文献:  3件

被引用文献を見るにはログインが必要です。ユーザIDをお持ちでない方は新規登録してください。

各種コード

  • NII論文ID(NAID)
    10018873854
  • NII書誌ID(NCID)
    AA11091750
  • 本文言語コード
    ENG
  • 資料種別
    ART
  • ISSN
    13238930
  • データ提供元
    CJP書誌  CJP引用  J-STAGE 
ページトップへ