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

Author

Listed:
  • Kouichi Ozaki

    (The Institute of Physical and Chemical Research (RIKEN))

  • Katsumi Inoue

    (Kokura Memorial Hospital)

  • Hiroshi Sato

    (Osaka University Graduate School of Medicine)

  • Aritoshi Iida

    (SNP Research Center, The Institute of Physical and Chemical Research (RIKEN))

  • Yozo Ohnishi

    (The Institute of Physical and Chemical Research (RIKEN))

  • Akihiro Sekine

    (SNP Research Center, The Institute of Physical and Chemical Research (RIKEN))

  • Hideyuki Sato

    (Osaka University Graduate School of Medicine)

  • Keita Odashiro

    (Kokura Memorial Hospital)

  • Masakiyo Nobuyoshi

    (Kokura Memorial Hospital)

  • Masatsugu Hori

    (Osaka University Graduate School of Medicine)

  • Yusuke Nakamura

    (SNP Research Center, The Institute of Physical and Chemical Research (RIKEN)
    Institute of Medical Science, University of Tokyo)

  • Toshihiro Tanaka

    (The Institute of Physical and Chemical Research (RIKEN))

Abstract

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)1. Functional variations in LTA are associated with susceptibility to MI2. Here we show that LTA protein binds to galectin-2, a member of the galactose-binding lectin family3. 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.

Suggested Citation

  • Kouichi Ozaki & Katsumi Inoue & Hiroshi Sato & Aritoshi Iida & Yozo Ohnishi & Akihiro Sekine & Hideyuki Sato & Keita Odashiro & Masakiyo Nobuyoshi & Masatsugu Hori & Yusuke Nakamura & Toshihiro Tanaka, 2004. "Functional variation in LGALS2 confers risk of myocardial infarction and regulates lymphotoxin-α secretion in vitro," Nature, Nature, vol. 429(6987), pages 72-75, May.
    • Handle: RePEc:nat:nature:v:429:y:2004:i:6987:d:10.1038_nature02502
    DOI: 10.1038/nature02502
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    Cited by:

    1. Han Zhang & Rahul Kalla & Jie Chen & Jianhui Zhao & Xuan Zhou & Alex Adams & Alexandra Noble & Nicholas T. Ventham & Judith Wellens & Gwo-Tzer Ho & Malcolm G. Dunlop & Jan Krzysztof Nowak & Yuan Ding , 2024. "Altered DNA methylation within DNMT3A, AHRR, LTA/TNF loci mediates the effect of smoking on inflammatory bowel disease," Nature Communications, Nature, vol. 15(1), pages 1-14, December.

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