| Project/Area Number |
18K09463
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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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| Review Section |
Basic Section 56060:Ophthalmology-related
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| Research Institution | St. Marianna University School of Medicine |
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Principal Investigator |
Ueno Hiroki 聖マリアンナ医科大学, 医学部, 講師 (30529897)
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| Co-Investigator(Kenkyū-buntansha) |
上野 聰樹 聖マリアンナ医科大学, 医学部, 名誉教授 (20109010)
服部 貴明 東京医科大学, 医学部, 兼任講師 (20408173)
鈴木 登 聖マリアンナ医科大学, 医学部, 教授 (40235982)
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| Project Period (FY) |
2018-04-01 – 2024-03-31
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| Project Status |
Completed (Fiscal Year 2023)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 糖尿病 / 角膜三叉神経 / 慢性炎症 / 角膜幹細胞 / マクロファージ |
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| Outline of Final Research Achievements |
Recent studies have gradually made it clear that a chronic inflammation and an activation of the immune system are involved in the pathogenesis of obesity-associated insulin resistance and type 2 diabetes. The purpose of this study is to evaluate the effects of corneal stem cells and corneal trigeminal nerve in terms of chronic low-grade inflammation in type 2 diabetes. The group of diabetic mice treated with subconjunctival injection of liposomal clodronate showed sub-epithelial corneal plexus similar to that of normal mice in terms of expression of βIII tubulin, a marker of nerves. These results suggest that macrophage-depleting drugs may protect against corneal sub-epithelial nerve plexus damage in severe type 2 diabetes when diabetic corneal damage occurs.
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| Academic Significance and Societal Importance of the Research Achievements |
慢性炎症状況下に置かれている角膜神経・角膜幹細胞に対する影響の解明は、重度糖尿病角膜症や混濁を伴う角膜ヘルペス等の角膜三叉神経関与疾患の治療を行う際に今後極めて有用である。幹細胞培養臓器移植は今後更に臨床応用されていく可能性を秘めているが、長期予後を考えた際幹細胞を維持し機能させる環境因子の補充だけでなく、炎症等の阻害因子の除外も重要である。本研究は特に慢性炎症という環境因子に注目し角膜三叉神経・角膜幹細胞を含んだニッチの機能維持を阻害する炎症メカニズムが解明できれば、幹細胞疲弊症の治療や自己幹細胞移植後の治療に繋がる可能性がある。
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