ATP结合盒载体A1的表达和阿波利波蛋白AI的结合在内密类型的动脉光滑肌细胞中受损
Hong Y Choi1, Maziar Rahmani, Brian W Wong
1Department of Medicine, Heart and Lung Institute, St. Paul's Hospital, 1081 Burrard Street, Vancouver, BC, Canada.
Circulation
|June 17, 2009
概括
在内脏光滑肌细胞 (SMCs) 中减少ATP结合盒载体A1 (ABCA1) 表达会损害胆固醇排泄,导致动脉样硬化中泡细胞的形成. 这表明ABCA1功能障碍是亲密SMC的关键.
科学领域:
- 心血管生物学 心血管生物学
- 动脉样硬化研究 动脉样硬化研究
- 细胞脂质代谢 细胞脂质代谢
背景情况:
- 动脉样硬化病变中的光滑肌细胞 (SMC) 积累胆固醇,形成泡细胞.
- 结合ATP的磁带载体A1 (ABCA1) 在细胞胆固醇排放中起着至关重要的作用.
研究的目的:
- 从模型和人类动脉样硬化动脉中研究ABCA1表达和活动的亲密和中间SMC.
- 了解ABCA1在光滑肌肉泡细胞形成中的作用.
主要方法:
- 在模型内密和介质SMC中比较ABCA1表达和脂质流量.
- 分析了人类动脉硬化冠状动脉内心和中间层的ABCA1水平.
- 评估了ABCA1上调对亲密SMC中的脂质处理的影响.
主要成果:
- 与中间的SMC相比,模型亲密的SMC表现出减少的ABCA1表达,受损的脂质排放,以及较差的阿波利波蛋白AI结合.
- 人类动脉样硬化亲密层显示ABCA1mRNA和蛋白质水平与中间层相比降低.
- 增强ABCA1表达并没有恢复内密SMC中的脂质流量或高密度脂蛋白形成,这表明缺乏必要的结合因子.
结论:
- 在模型和人体亲密SMC中,ABCA1的表达显著减少.
- 在亲密的SMC中ABCA1活动受损,有助于胆固醇的积累和泡细胞的形成.
- 最终的SMC可能缺乏ABCA1介导胆固醇流动所需的关键因素.
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