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

Miyako Tanaka, Kenji Ikeda, Takayoshi Suganami (), Chikara Komiya, Kozue Ochi, Ibuki Shirakawa, Miho Hamaguchi, Satoshi Nishimura, Ichiro Manabe, Takahisa Matsuda, Kumi Kimura, Hiroshi Inoue, Yutaka Inagaki, Seiichiro Aoe, Sho Yamasaki and Yoshihiro Ogawa ()
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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
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
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

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: 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.

Date: 2014
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DOI: 10.1038/ncomms5982

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