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Macrophage-inducible C-type lectin underlies obesity-induced adipose tissue fibrosis

Author

Listed:
  • Miyako Tanaka

    (Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University)

  • Kenji Ikeda

    (Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University)

  • Takayoshi Suganami

    (Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University
    Japan Science and Technology Agency, PRESTO)

  • Chikara Komiya

    (Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University)

  • Kozue Ochi

    (Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University)

  • Ibuki Shirakawa

    (Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University)

  • Miho Hamaguchi

    (Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University)

  • Satoshi Nishimura

    (The University of Tokyo
    Translational Systems Biology and Medicine Initiative, The University of Tokyo
    Jichi Medical University)

  • Ichiro Manabe

    (The University of Tokyo)

  • Takahisa Matsuda

    (Takeda Pharmaceutical Company)

  • Kumi Kimura

    (Brain/Liver Interface Medicine Research Center, Kanazawa University)

  • Hiroshi Inoue

    (Brain/Liver Interface Medicine Research Center, Kanazawa University)

  • Yutaka Inagaki

    (Center for Matrix Biology and Medicine, Tokai University School of Medicine)

  • Seiichiro Aoe

    (Otsuma Women’s University)

  • Sho Yamasaki

    (Medical Institute of Bioregulation, Kyushu University)

  • Yoshihiro Ogawa

    (Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University)

Abstract

In obesity, a paracrine loop between adipocytes and macrophages augments chronic inflammation of adipose tissue, thereby inducing systemic insulin resistance and ectopic lipid accumulation. Obese adipose tissue contains a unique histological structure termed crown-like structure (CLS), where adipocyte-macrophage crosstalk is known to occur in close proximity. Here we show that Macrophage-inducible C-type lectin (Mincle), a pathogen sensor for Mycobacterium tuberculosis, is localized to macrophages in CLS, the number of which correlates with the extent of interstitial fibrosis. Mincle induces obesity-induced adipose tissue fibrosis, thereby leading to steatosis and insulin resistance in liver. We further show that Mincle in macrophages is crucial for CLS formation, expression of fibrosis-related genes and myofibroblast activation. This study indicates that Mincle, when activated by an endogenous ligand released from dying adipocytes, is involved in adipose tissue remodelling, thereby suggesting that sustained interactions between adipocytes and macrophages within CLS could be a therapeutic target for obesity-induced ectopic lipid accumulation.

Suggested Citation

  • Miyako Tanaka & Kenji Ikeda & Takayoshi Suganami & Chikara Komiya & Kozue Ochi & Ibuki Shirakawa & Miho Hamaguchi & Satoshi Nishimura & Ichiro Manabe & Takahisa Matsuda & Kumi Kimura & Hiroshi Inoue &, 2014. "Macrophage-inducible C-type lectin underlies obesity-induced adipose tissue fibrosis," Nature Communications, Nature, vol. 5(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5982
    DOI: 10.1038/ncomms5982
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    Cited by:

    1. Jing Yan & Yuemei Zhang & Hairong Yu & Yicen Zong & Daixi Wang & Jiangfei Zheng & Li Jin & Xiangtian Yu & Caizhi Liu & Yi Zhang & Feng Jiang & Rong Zhang & Xiangnan Fang & Ting Xu & Mingyu Li & Jianzh, 2022. "GPSM1 impairs metabolic homeostasis by controlling a pro-inflammatory pathway in macrophages," Nature Communications, Nature, vol. 13(1), pages 1-22, December.

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