Macrophage-inducible C-type lectin underlies obesity-induced adipose tissue fibrosis
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 adipocy...
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| Veröffentlicht in: | Nature communications 2014-09, Vol.5 (1), p.4982-4982, Article 4982 |
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| creator | Tanaka, Miyako Ikeda, Kenji Suganami, Takayoshi Komiya, Chikara Ochi, Kozue Shirakawa, Ibuki Hamaguchi, Miho Nishimura, Satoshi Manabe, Ichiro Matsuda, Takahisa Kimura, Kumi Inoue, Hiroshi Inagaki, Yutaka Aoe, Seiichiro Yamasaki, Sho Ogawa, Yoshihiro |
| description | 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.
The protein Mincle can sense pathogens and molecules associated with cell death. Here the authors show that Mincle expressed in macrophages is a mediator of obesity-induced fibrosis and inflammation of adipose tissue, and that Mincle knockout mice are protected from diet-induced metabolic dysfunction. |
| doi_str_mv | 10.1038/ncomms5982 |
| format | Article |
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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.
The protein Mincle can sense pathogens and molecules associated with cell death. Here the authors show that Mincle expressed in macrophages is a mediator of obesity-induced fibrosis and inflammation of adipose tissue, and that Mincle knockout mice are protected from diet-induced metabolic dysfunction.</description><identifier>ISSN: 2041-1723</identifier><identifier>EISSN: 2041-1723</identifier><identifier>DOI: 10.1038/ncomms5982</identifier><identifier>PMID: 25236782</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/250/2504/342 ; 692/420 ; 692/699/2743/393 ; Adipocytes - cytology ; Adipose tissue ; Adipose Tissue - metabolism ; Adipose Tissue - physiopathology ; Animals ; Body fat ; Fibrosis ; Humanities and Social Sciences ; Inflammation - metabolism ; Insulin Resistance ; Lectins, C-Type - metabolism ; Ligands ; Lipids - chemistry ; Liver - metabolism ; Macrophages - cytology ; Macrophages - metabolism ; Male ; Membrane Proteins - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; multidisciplinary ; Obesity ; Obesity - metabolism ; Receptors, Cell Surface - metabolism ; RNA, Messenger - metabolism ; Science ; Science (multidisciplinary)</subject><ispartof>Nature communications, 2014-09, Vol.5 (1), p.4982-4982, Article 4982</ispartof><rights>Springer Nature Limited 2014</rights><rights>Copyright Nature Publishing Group Sep 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-ba8efbb03ce25149017b49d9481eb77e0b456737a71e5aa1f7798f1631f69cce3</citedby><cites>FETCH-LOGICAL-c387t-ba8efbb03ce25149017b49d9481eb77e0b456737a71e5aa1f7798f1631f69cce3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/ncomms5982$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://doi.org/10.1038/ncomms5982$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41096,42165,51551</link.rule.ids><linktorsrc>$$Uhttps://doi.org/10.1038/ncomms5982$$EView_record_in_Springer_Nature$$FView_record_in_$$GSpringer_Nature</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25236782$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tanaka, Miyako</creatorcontrib><creatorcontrib>Ikeda, Kenji</creatorcontrib><creatorcontrib>Suganami, Takayoshi</creatorcontrib><creatorcontrib>Komiya, Chikara</creatorcontrib><creatorcontrib>Ochi, Kozue</creatorcontrib><creatorcontrib>Shirakawa, Ibuki</creatorcontrib><creatorcontrib>Hamaguchi, Miho</creatorcontrib><creatorcontrib>Nishimura, Satoshi</creatorcontrib><creatorcontrib>Manabe, Ichiro</creatorcontrib><creatorcontrib>Matsuda, Takahisa</creatorcontrib><creatorcontrib>Kimura, Kumi</creatorcontrib><creatorcontrib>Inoue, Hiroshi</creatorcontrib><creatorcontrib>Inagaki, Yutaka</creatorcontrib><creatorcontrib>Aoe, Seiichiro</creatorcontrib><creatorcontrib>Yamasaki, Sho</creatorcontrib><creatorcontrib>Ogawa, Yoshihiro</creatorcontrib><title>Macrophage-inducible C-type lectin underlies obesity-induced adipose tissue fibrosis</title><title>Nature communications</title><addtitle>Nat Commun</addtitle><addtitle>Nat Commun</addtitle><description>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.
The protein Mincle can sense pathogens and molecules associated with cell death. Here the authors show that Mincle expressed in macrophages is a mediator of obesity-induced fibrosis and inflammation of adipose tissue, and that Mincle knockout mice are protected from diet-induced metabolic dysfunction.</description><subject>631/250/2504/342</subject><subject>692/420</subject><subject>692/699/2743/393</subject><subject>Adipocytes - cytology</subject><subject>Adipose tissue</subject><subject>Adipose Tissue - metabolism</subject><subject>Adipose Tissue - physiopathology</subject><subject>Animals</subject><subject>Body fat</subject><subject>Fibrosis</subject><subject>Humanities and Social Sciences</subject><subject>Inflammation - metabolism</subject><subject>Insulin Resistance</subject><subject>Lectins, C-Type - metabolism</subject><subject>Ligands</subject><subject>Lipids - chemistry</subject><subject>Liver - metabolism</subject><subject>Macrophages - cytology</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Membrane Proteins - 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Academic</collection><jtitle>Nature communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Tanaka, Miyako</au><au>Ikeda, Kenji</au><au>Suganami, Takayoshi</au><au>Komiya, Chikara</au><au>Ochi, Kozue</au><au>Shirakawa, Ibuki</au><au>Hamaguchi, Miho</au><au>Nishimura, Satoshi</au><au>Manabe, Ichiro</au><au>Matsuda, Takahisa</au><au>Kimura, Kumi</au><au>Inoue, Hiroshi</au><au>Inagaki, Yutaka</au><au>Aoe, Seiichiro</au><au>Yamasaki, Sho</au><au>Ogawa, Yoshihiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Macrophage-inducible C-type lectin underlies obesity-induced adipose tissue fibrosis</atitle><jtitle>Nature communications</jtitle><stitle>Nat Commun</stitle><addtitle>Nat Commun</addtitle><date>2014-09-19</date><risdate>2014</risdate><volume>5</volume><issue>1</issue><spage>4982</spage><epage>4982</epage><pages>4982-4982</pages><artnum>4982</artnum><issn>2041-1723</issn><eissn>2041-1723</eissn><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.
The protein Mincle can sense pathogens and molecules associated with cell death. Here the authors show that Mincle expressed in macrophages is a mediator of obesity-induced fibrosis and inflammation of adipose tissue, and that Mincle knockout mice are protected from diet-induced metabolic dysfunction.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>25236782</pmid><doi>10.1038/ncomms5982</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 631/250/2504/342 692/420 692/699/2743/393 Adipocytes - cytology Adipose tissue Adipose Tissue - metabolism Adipose Tissue - physiopathology Animals Body fat Fibrosis Humanities and Social Sciences Inflammation - metabolism Insulin Resistance Lectins, C-Type - metabolism Ligands Lipids - chemistry Liver - metabolism Macrophages - cytology Macrophages - metabolism Male Membrane Proteins - metabolism Mice Mice, Inbred C57BL Mice, Knockout multidisciplinary Obesity Obesity - metabolism Receptors, Cell Surface - metabolism RNA, Messenger - metabolism Science Science (multidisciplinary) |
| title | Macrophage-inducible C-type lectin underlies obesity-induced adipose tissue fibrosis |
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