| Project/Area Number |
26460491
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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 |
Experimental pathology
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
池田 康博 九州大学, 医学研究院, 准教授 (20380389)
米満 吉和 九州大学, 薬学研究院, 教授 (40315065)
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| Co-Investigator(Renkei-kenkyūsha) |
Ikeda Yasuhiro 九州大学, 医学研究院, 准教授 (20380389)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | tie / angiopoietin / 血管新生 / 糖尿病 / 微小血管障害 / Angiopoietin / Tie / 血管生物学 / 血管内皮細胞 / 可溶型変換 / Tie受容体 |
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| Outline of Final Research Achievements |
In this study, we investigate the biological/biochemical role of Tie-1 shedding in the angiopoietin (Ang)/Tie system in human endothelial cells. Experimental data obtained through this study suggest that the two types of glycosylation-dependent full length Tie-1 play biologically/biochemically different roles in the Ang/Tie system, and PKC-dependent rapid Tie-1 shedding might act as an angiogenic switch via a change of signal balance between Tie-2 and Tie-1. Failure of the PKC-dependent Tie-1/Tie-2 system, based on increase in level of endothelial PKC activation in diabetes mellitus, may facilitate inducing microvasculopathy.
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