A Basic Research for Constructing a Treatment for Diabetic Kidney Disease by Endocan, a Endothelial specific moelcule.
| Project/Area Number |
16K09636
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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 | Kawasaki Medical School |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
柏原 直樹 川崎医科大学, 医学部, 教授 (10233701)
佐藤 稔 川崎医科大学, 医学部, 准教授 (70449891)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 糖鎖異常 / 糸球体内皮 / 糖尿病性腎症 / 血管新生 / 糖タンパク / デルマタン硫酸 / エンドカン / 血管内皮 / プロテオグリカン / 糖尿病 |
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| Outline of Final Research Achievements |
Synthetic endocan and endoglycan without glycan (glycan deficient type) were expressed in cultured cells from kidney. These were collected from the supernatant of the cells. These did not affect cell proliferation, cell death, cell migration, or angiogenesis on renal glomerular endothelial cells or renal mesangial cells (special cells present in renal glomeruli). Costimulation with vascular endothelial growth factor also had no effect. On the other hand, when the NO signal decreased, endocan expression did not increase in vascular endothelial cells, but when oxidative stress increased, endocan expression increased.
We tried to create a mouse that overexpresses endocan gene specifically in the vascular endothelium, but the gene expression level was too low to use in experiments.
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| Academic Significance and Societal Importance of the Research Achievements |
エンドカンは血管内皮細胞で作られ，可溶性の特殊な構造をもつ糖とタンパク質の複合体である．その血中レベルは敗血症の重症度と相関し，内皮障害の信頼できるバイオマーカーと考えられている．慢性腎臓病患者では，エンドカンの血中濃度が増加し，エンドカンの増加は心血管イベント発症と相関することが報告されている．この研究では，エンドカン発現増加には血管内皮細胞への一酸化窒素によるシグナル低下よりも酸化ストレス亢進の方が大きく影響していることを明らかにした．エンドカンが，酸化ストレスが亢進している糖尿病性腎症の治療標的となる可能性があり，社会的意義が大きい．
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Report
(4 results)
Research Products
(6 results)
