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通过DOCK4驱动内皮细胞LDL转细胞,促进动脉样硬化

Linzhang Huang¹, Ken L Chambliss¹, Xiaofei Gao^2,3,4,5

¹Center for Pulmonary and Vascular Biology, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.

|April 26, 2019

概括

内皮细胞中的扫除受体SR-B1积极地将LDL胆固醇输入动脉壁,促进动脉样硬化. 这一发现挑战了被动LDL的进入,并提出了心血管疾病的新治疗点.

科学领域:

心血管生物学
内皮细胞生物学
动脉样硬化研究

背景情况:

动脉样硬化是心脏病发作和中风的主要原因, 起始于低密度脂蛋白 (LDL) 胆固醇进入动脉壁.
这种LDL进入动脉壁的确切机制尚不完全理解.

研究的目的:

调查内皮细胞中吸收受体类B型1 (SR-B1) 在调解LDL进入动脉中的作用.
阐明SR-B1促进LDL转移和促进动脉样硬化的分子机制.

主要方法:

用小鼠模型评估内皮细胞中的SR-B1功能.
对LDL和SR-B1的体内同位化研究.
研究SR-B1,细胞动力学4 (DOCK4) 和RAC1信号之间的相互作用.
在小鼠和人类动脉硬化动脉中分析SR-B1和DOCK4表达.

主要成果:

内皮SR-B1调节了LDL输入动脉和巨细胞的积累,从而导致动脉样硬化.
LDL 颗粒与内皮细胞内囊泡中的 SR- B1 结合.
通过SR-B1介导的LDL转细胞化需要直接结合和特定的细胞质域与DOCK4相互作用,从而激活RAC1.
在动脉样硬化易发的区域和人类动脉样硬化动脉中,SR- B1和DOCK4的表达上调.

结论:

内皮SR-B1积极地将LDL输入动脉壁,挑战动脉生成的被动扩散模型.
通过SR- B1抑制向内皮的LDL输送,为心血管疾病提供了一个新的治疗策略.

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