| Project/Area Number |
24659119
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
General pharmacology
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KITASATO Hidero 北里大学, 医療衛生学部, 教授 (90195256)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | プロスタノイド / リンパ管新生 / ホメオスタシス / 体液 / 高血圧 / 炎症 / LPS / COX-2 / 腹水 / アラキドン酸代謝物 / COX / PGE合成酵素 / 皮下組織 / ナトリウム / Lyve-1 / VEGF-C / 食塩 |
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| Outline of Final Research Achievements |
We had tested the roles of an inducible prostaglandin E synthase, mPGES-1 in facilitation of inflammation-induced lymphangiogenesis (IL) elicited by lipopollysccharide (LPS). With LPS i.p. injections, lymphatics in diaphragm were widened and Lyve-1-positive ladder-structured lymphatics were increased temporally in comparison with vehicle-treated wild type mice (WT). This increase of lymphangiogenesis was accompanied with increased expressions of vascular endothelial growth factor (VEGF)-C/D. In mPGES-1 knockout mice (KO), IL was suppressed with reduced expressions of VEGF-C/D. When FITC-dextran was injected into peritoneal cavities, the residual amount of FITC-dextran was reduced significantly in WT with LPS treatment. This reduction was significantly restored in mPGES-1 KO. These results suggested that mPGES-1 had significant roles in facilitation of lymphangiogenesis active in fluid drainage during IL, and that this enzyme will be a novel target for controlling IL.
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