| Project/Area Number |
17K09681
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Hirosaki University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
島田 美智子 弘前大学, 医学研究科, 講師 (40463765)
田中 完 弘前大学, 教育学部, 教授 (50271820)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 糸球体血管内皮細胞 / endothelial cells / ISGs / TLR3 / 慢性腎臓病 / メサンギウム細胞 / 血管内皮細胞 |
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| Outline of Final Research Achievements |
It is known that innate immunity is involved in the pathogenesis of chronic renal diseases. However, the molecular mechanisms by which induce chronic renal diseases have not been fully clarified. We found that treatment of cultured human glomerular endothelial cells with poly IC, which mimics viral infection via a receptor named Toll-like receptor 3 (TLR3), induces the expression of PAI-1 which induces thrombosis, a potent proinflammatory cytokine IL-6, and neutrophils chemoattractants CXCL1 and CX3CL1. These finding suggests that TLR3 signaling may be involved in innate immune and inflammatory reactions in chronic renal diseases.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究の成果は、慢性腎臓病の病態における免疫系の関与に関する新たな知見を見出しており、慢性腎臓病の新たな治療戦略の構築に向けた、基盤となるデータが得られたと考えている。慢性腎臓病は、慢性腎不全に進行することも少なくなく、慢性腎不全になると透析医療の適応となり、様々な心血管や運動器の合併症の発生や、QOL の低下が問題となる上、高額な医療費も必要となる。本研究の成果は、慢性腎臓病の新たな切り口による治療法の開発の基盤となる可能性があり、透析導入を少しでも遅らせ、慢性腎臓病患者の QOL 改善や、ひいては、医療費の削減につながる可能性もある。
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