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在巨细胞和动脉样硬化斑块中,SR-B1和S1PR1之间的依赖体相互作用

Christine Bassila¹, George E G Kluck¹, Narmadaa Thyagarajan¹

¹Department of Biochemistry and Biomedical Sciences, Thrombosis and Atherosclerosis Research Institute, Hamilton Health Sciences, McMaster University, Hamilton, ON, Canada.

Journal of lipid research

|April 7, 2024

概括

高密度脂蛋白 (HDL) 通过吸尘器受体B类,I型 (SR-B1) 和基-1-酸盐受体1 (S1PR1) 发出信号. 这项研究表明SR-B1和S1PR1在巨细胞和动脉样硬化斑块中物理相互作用,由HDL相关的S1P介导.

科学领域:

心血管生物学心血管生物学
脂质代谢脂质代谢是什么
分子细胞生物学分子细胞生物学

背景情况:

高密度脂蛋白 (HDL) 在逆胆固醇运输中发挥作用,并具有动脉动脉保护性.
高脂介导的信号传递涉及黄-1-酸盐 (S1P) 和其受体,包括黄-1-酸盐受体1 (S1PR1).
拾尸体受体类B,I型 (SR-B1) 是一个关键的HDL受体,涉及到HDL信号传输.

研究的目的:

为了研究SR-B1和S1PR1在原发性巨细胞和动脉样硬化斑块中的物理相互作用.
确定HDL相关S1P在调解SR-B1和S1PR1复合体形成中的作用.
阐明SR-B1/S1PR1复合体形成在动脉保护信号传输中的功能后果.

主要方法:

使用表达eGFP标记S1PR1 (S1pr1^eGFP/eGFP) 的试验小鼠.
采用近距离结合分析来检测培养的巨细胞和小鼠动脉样硬化斑块中的SR-B1/S1PR1相互作用.
使用S1P,SR-B1抑制剂,S1PR1激动剂 (SEW2871) 和S1PR1对抗剂 (Ex26) 来评估相互作用依赖性.

主要成果:

证明HDL刺激了原发性巨细胞中SR-B1和S1PR1之间的物理相互作用.
证实这种相互作用依赖于HDL相关的S1P,并且可以通过SR-B1脂质转移活性和S1PR1信号调节.
在S1pr1^eGFP/eGFP小鼠的动脉样性斑块中观察到丰富的SR-B1/S1PR1复合体,这些S1pr1^eGFP/eGFP小鼠的动脉样性斑块被S1PR1抗剂治疗破坏.

结论:

在巨细胞和动脉样硬化斑块中,SR-B1和S1PR1形成依赖于连接体的复合体.
这种相互作用对于调解参与动脉膜保护的高密度胆固醇信号通路至关重要.
提供了对SR-B1和S1PR1在心血管健康中的作用的机制性见解.

关键词:

动脉样硬化动脉样硬化高密度脂蛋白是一种高密度脂蛋白.巨细胞是一个巨细胞.拾尸体受体类B型I类受体斯芬戈-1-酸盐是一种酸盐.斯芬戈-1-酸盐受体 1 种

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