Role of a novel pathogen sensor in the pathophysiology of acute renal failure
| Project/Area Number |
23659440
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Kidney internal medicine
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
SUGANAMI Takayoshi 東京医科歯科大学, 大学院・医歯学総合研究科, 寄附講座教授 (50343752)
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| Co-Investigator(Renkei-kenkyūsha) |
瀬藤 光利 浜松医科大学, 分子イメージング先端研究センター, 教授 (20302664)
山崎 晶 九州大学, 生体防御医学研究所, 教授 (40312946)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 腎虚血再灌流障害 / マクロファージ / 急性腎不全 / 炎症 / 腎虚血再灌流傷害 / C型レクチン / Toll様受容体 |
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| Research Abstract |
Accumulating evidence suggests that pathogen sensors such as TLRs and C-type lectin families are capable of sensing endogenous ligands released from damaged and stressed cells and tissues, thereby inducing sterile inflammation. Here we demonstrate that macrophage-inducible C-typelectin (Mince) is involved in the pathophysiology of renal ischemia-reperfusion injury, an experimental model of acute renal failure. Our data also suggest that Mincle is mainly expressed in proinflammatory macrophages that infiltrate into the damaged kidney.
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Report
(3 results)
Research Products
(8 results)
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[Journal Article] Increased expression of macrophage-inducible C-type lectin in adipose tissue of obese mice and humans2011
Author(s)
M. Ichioka, T. Suganami, N. Tsuda, I. Shirakawa, Y. Hirata, N. Satoh-Asahara, Y. Shimoda, M. Tanaka, M. Kim-Saijo, Y. Miyamoto, Y. Kamei, M. Sata, Y. Ogawa
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Journal Title
Diabetes
Volume: 60
Issue: 3
Pages: 819-826
DOI
Related Report
Peer Reviewed
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