Functional variation in LGALS2 confers risk of myocardial infarction and regulates lymphotoxin-α secretion in vitro

Kouichi Ozaki, Katsumi Inoue, Hiroshi Sato, Aritoshi Iida, Yozo Ohnishi, Akihiro Sekine, Hideyuki Sato, Keita Odashiro, Masakiyo Hobuyoshi, Masatsugu Hori, Yusuko Nakamura, Toshihiro Tanaka

研究成果: ジャーナルへの寄稿学術誌査読

222 被引用数 (Scopus)

抄録

Myocardial infarction (MI) has become one of the leading causes of death in the world. Its pathogenesis includes chronic formation of plaque inside the vessel wall of the coronary artery and acute rupture of the artery, implicating a number of inflammation-mediating molecules, such as the cytokine lymphotoxin-α (LTA). Functional variations in LTA are associated with susceptibility to MI. Here we show that LTA protein binds to galectin-2, a member of the galactose-binding lectin family. Our case-control association study in a Japanese population showed that a single nucleotide polymorphism in LGALS2 encoding galectin-2 is significantly associated with susceptibility to MI. This genetic substitution affects the transcriptional level of galectin-2 in vitro, potentially leading to altered secretion of LTA, which would then affect the degree of inflammation; however, its relevance to other populations remains to be clarified. Smooth muscle cells and macrophages in the human atherosclerotic lesions expressed both galectin-2 and LTA. Our findings thus suggest a link between the LTA cascade and the pathogenesis of MI.

本文言語英語
ページ(範囲)72-75
ページ数4
ジャーナルNature
429
6987
DOI
出版ステータス出版済み - 5月 6 2004
外部発表はい

!!!All Science Journal Classification (ASJC) codes

  • 一般

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