| Literature DB >> 25236782 |
Miyako Tanaka1, Kenji Ikeda1, Takayoshi Suganami2, Chikara Komiya1, Kozue Ochi1, Ibuki Shirakawa3, Miho Hamaguchi1, Satoshi Nishimura4, Ichiro Manabe5, Takahisa Matsuda6, Kumi Kimura7, Hiroshi Inoue7, Yutaka Inagaki8, Seiichiro Aoe9, Sho Yamasaki10, Yoshihiro Ogawa1.
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.Entities:
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Year: 2014 PMID： 25236782 DOI： 10.1038/ncomms5982
Source DB: PubMed Journal: Nat Commun ISSN： 2041-1723 Impact factor: 14.919