| Project/Area Number |
25670439
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Endocrinology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
OGAWA Yoshihiro 東京医科歯科大学, 医歯(薬)学総合研究科, 教授 (70291424)
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| Co-Investigator(Kenkyū-buntansha) |
YAMASAKI Sho 九州大学, 生体防御医学研究所, 教授 (40312946)
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| Co-Investigator(Renkei-kenkyūsha) |
TANAKA Miyako 東京医科歯科大学, 大学院医歯(薬)学総合研究科, メディカルフェロー (60622793)
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| Project Period (FY) |
2013-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
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| Keywords | 線維化 / マクロファージ / Mincle / 脂肪組織 / 線維芽細胞 / crown-like structure / 肥満 / 細胞死 |
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| Research Abstract |
Fibrosis is a final, common pathological outcome of a variety of chronic inflammatory diseases. In this study, we focused on Macrophage-inducible C-type lectin (Mincle), a pathogen sensor that recognizes Mycobacterium tuberculosis and is induced in obese adipose tissue and investigated the role of Mincle in the regulation of adipose tissue fibrosis. In the obese adipose tissue, Mincle was expressed mainly in proinflammatory M1 macrophages. Mincle stimulation caused the upregulation of genes related to fibrogenesis in peritoneal macrophages. Furthermore, Mincle stimulation by trehalose 6,6'-dimycolate, an exogenous ligand for Mincle, in adipose tissue resulted in adipose tissue fibrosis. These observations suggest that Mincle activation in obese adipose tissue leads to the progression of adipose tissue fibrosis, thereby suggesting that Mincle antagonism offers an novel anti-fibrotic therapy for chronic fibrotic diseases.
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