| Project/Area Number |
26460362
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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 |
General medical chemistry
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| Research Institution | University of Yamanashi |
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Principal Investigator |
INOUE Osamu 山梨大学, 総合研究部, 准教授 (00432154)
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| Co-Investigator(Kenkyū-buntansha) |
井上 克枝 山梨大学, 総合研究部, 教授 (10324211)
尾崎 由基男 山梨大学, 総合研究部, 医学研究員 (30134539)
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| Research Collaborator |
OOTAKE Shimon
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | CLEC-2 / 血管新生 / 炎症 / DSS / リンパ管 / チオグリコネート |
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| Outline of Final Research Achievements |
The role of cellular CLEC-2 in lymphangiogenesis at the site of inflammation was investigated. In this study, 3% Dextran Sulfate Sodium (DSS)-induced enterocolitis mice were used. CLEC-2 expression was completely terminated by injection of anti-CLEC-2 antibody intraperitoneally. There was no significant difference in clinical manifestations, severity of inflammation, gut weight, or density of lymphatic vessels at the site of inflammation in the presence or absence of CLEC-2. Density of blood vessels at the site of inflammation was significantly decreased. Since the density of blood vessels was decreased while that of lymphatic vessels was not in cellular CLEC-2 terminated mice, it it obvious that CLEC-2 plays a role in angiogenesis at the site of inflammation.
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