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酸化されたLDLは,Akt/endothelial nitric oxide synthase経路に対する抑制作用によって,血管内皮成長因子誘発の内皮細胞移動を阻害する

E Chavakis¹, E Dernbach, C Hermann

¹Department of Internal Medicine IV, University of Frankfurt, Germany.

|April 25, 2001

まとめ

酸化LDL (oxLDL) は,Akt/eNOS経路を阻害し,酸化窒素 (NO) の生成を減少させることで,内皮細胞の移動を損なう. AktまたはeNOS機能を復元すると,oxLDLが誘発したこの抑制が逆転する.

科学分野:

内皮細胞生物学エンドセル細胞生物学
血管機能の分子メカニズム
脂質代謝と心血管疾患について

背景:

酸化低密度リポプロテイン (oxLDL) は,内皮細胞 (EC) 移動を阻害することが知られている.
血管内皮成長因子 (VEGF) は,Akt/タンパク質キナーゼB経路経由でEC移動を刺激し,内皮酸化窒素合成酵素 (eNOS) の活性化と酸化窒素 (NO) の生成につながります.

研究の目的:

oxLDLがEC移行を阻害するメカニズムを調査する.
oxLDLがAkt/eNOS経路およびその後のNO生成に影響するかどうかを判断する.

主な方法:

EC移住を評価するために,インビトロ"傷口傷口分析"を行います.
Aktのリン酸化状態を評価するためのウエスタン・ブロット分析.
光インジケーターを使用して,NO生産の定量化.
構成的に活性なAktとフォスフォミメティックなeNOS構造物の過剰表現.

主要な成果:

oxLDLは,VEGF誘発EC移行を,用量依存的に抑制した.
oxLDLは,Aktの脱リン酸化と無活性化を引き起こしました.
oxLDLは,VEGF誘発 NO生成を減少させた.
AktまたはeNOSの過剰発現は,oxLDLの抑制効果を逆転させた.

結論:

oxLDLは,Aktを脱酸化することによってEC移行を阻害し,eNOSの活性化を阻害します.
Akt/eNOS信号伝達の障害によるNO濃度の低下は,EC移行に対するoxLDLの抑制効果を媒介する.

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