Development of the new angiogenic inhibitor targeting HMGB-1
| Project/Area Number |
15K18996
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General pharmacology
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| Research Institution | Kindai University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | マクロファージ / 血管新生 / 炎症性メディエーター / インターロイキン-18 / オステオポンチン / トロンビン / CD163 / 細胞間相互作用 |
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| Outline of Final Research Achievements |
Macrophages (Mφs) are classified as M1 or M2 phenotypes, with the latter promoting angiogenesis which is a precipitating factor for several chronic inflammatory diseases including rheumatoid arthritis (RA) and various cancers. In this study, we initially established the simplified in vitro experimental model to evaluate the influence of micromilieu on the Mφ polarization status, morphology, and functional activity. As a result, M2-like Mφ strongly induced excessive angiogenesis through the direct cell-cell interaction with endothelial cells mediated by the surface CD163.
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Report
(4 results)
Research Products
(7 results)
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[Journal Article] Interleukin-18 Amplifies Macrophage Polarization and Morphological Alteration, Leading to Excessive Angiogenesis.2018
Author(s)
Kobori T, Hamasaki S, Kitaura A, Yamazaki Y, Nishinaka T, Niwa A, Nakao S, Wake H, Mori S, Yoshino T, Nishibori M, Takahashi H
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Journal Title
Frontiers in Immunology
Volume: 9
Pages: 334-334
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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