Investigation of ANGPTL2 involvement in pathogenesis of age-related macular degeneration.
Project/Area Number |
25462734
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Ophthalmology
|
Research Institution | Keio University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
OZAWA YOKO 慶應義塾大学, 医学部, 講師 (90265885)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | アンギオポイエチン様タンパク / 加齢黄斑変性 / 脈絡膜新生血管 / マクロファージ / アンギオポイエチン様蛋白 / 炎症性サイトカイン |
Outline of Final Research Achievements |
ANGPTL2 was localized at lesion of laser-induced choroidal neovascularization in mice, and reduction of CNV volume and CNV-induced pro-inflammatory mediators were observed at ANGPTL2 deficient mice, indicating involvement of ANGPTL2 in CNV pathogenesis. In bone marrow transplantation model, both ANGPTL2 from retinal tissue and macrophage participated CNV development. In vitro study, phosphorylation of NF-κB and ERK1/2, acceleration of pro-inflammatory mediators, and macrophage migration were driven by recombinant ANGPTL2; suppressed by integrin α4 and/or β2 neutralizing antibody. ANGPTL2 and its signal induction might be new therapeutic target against age-related macular degeneration.
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Report
(4 results)
Research Products
(14 results)