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KAKEN_25462734seika.pdf
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:451.9 KB
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| Title |
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加齢黄斑変性の病態におけるAngptl2の意義の解析
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| Kana |
カレイ オウハン ヘンセイ ノ ビョウタイ ニ オケル Angptl2 ノ イギ ノ カイセキ
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Karei ohan hensei no byotai ni okeru Angptl2 no igi no kaiseki
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Investigation of ANGPTL2 involvement in pathogenesis of age-related macular degeneration.
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平沢, 学
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ヒラサワ, マナブ
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Hirasawa, Manabu
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慶應義塾大学・医学部・共同研究員
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Research team head
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科研費研究者番号 : 80365345
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小沢, 洋子
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オザワ, ヨウコ
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Ozawa, Yoko
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慶應義塾大学・医学部・講師
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Research team member
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科研費研究者番号 : 90265885
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2016
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科学研究費補助金研究成果報告書
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2015
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ANGPTL2はマウスレーザー脈絡膜新生血管(CNV)病変部に局在し, ANGPTL2欠損マウスではCNV容積と炎症性メディエーター発現の抑制を認め, ANGPTL2のCNV病態への関与が示唆された。骨髄移植モデルでは, 網膜組織ならびにマクロファージ双方由来のANGPTL2がCNV形成に関与していた。培養マクロファージでは, ANGPTL2添加でERK1/2とNF-κBのリン酸化, 炎症性メディエーターの発現亢進, およびクロファージ遊走促進を認め, それらはインテグリンα4およびβ2中和交代によって抑制された。ANGPTL2はCNV治療の新たなターゲットとして期待される。
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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研究種目 : 基盤研究(C)(一般)
研究期間 : 2013～2015
課題番号 : 25462734
研究分野 : 眼科学
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