LOX-1介导oxLDL内吞致内皮功能紊乱的分子机制
基本信息
结项摘要
内皮功能紊乱是动脉粥样硬化（AS）发生过程中最早和最有决定性的事件之一。氧化低密度脂蛋白（oxLDL）导致内皮功能紊乱是不争的事实。凝集素样氧化低密度脂蛋白受体（LOX-1）是内皮细胞膜上特异性识别摄取oxLDL的最主要受体。oxLDL可通过激活LOX-1进而活化MAPK和PKC途径而导致内皮功能紊乱，但LOX-1胞内段很短，无SH2结构域，亦不与G蛋白偶联，其激活MAPK和PKC途径的机制尚不清楚。我们的研究显示：内皮细胞膜上LOX-1与Caveolin-1共定位，且LOX-1与Caveolin-1、Annexin-2免疫共沉淀，提示这三者可能存在相互作用。我们拟采用缺失突变体构建、siRNA、荧光共振能量转移技术（FRET）等方法，明确LOX-1与Caveolin-1、Annexin-2是否相互作用，并探讨这种相互作用对LOX-1介导oxLDL内吞过程中导致内皮功能紊乱的分子机制。
项目摘要
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数据更新时间：2023-05-31
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