暴露于雌激素会增加人体单细胞对血管内皮的粘附和血管细胞粘附分子-1-1的内皮细胞表达
J A McCrohon1, W Jessup, D J Handelsman
1Heart Research Institute, Departments of Cardiology and Andrology, Royal Prince Alfred Hospital, Sydney, Australia. janem@card.rpa.cs.nsw.gov.au
Circulation
|May 5, 1999
概括
像二测试 (DHT) 这样的雄激素会增加单细胞对内皮细胞的粘附,这是动脉样硬化的一个关键步骤. 这种效应是由血管细胞粘附分子-1 (VCAM-1) 介导的,可以通过雄激素受体抑制剂来阻断.
科学领域:
- 内分泌学 在内分泌学.
- 心血管生物学 心血管生物学
- 免疫学 免疫学 免疫学
背景情况:
- 男性性别是冠状动脉疾病 (CAD) 的已知危险因素.
- 单细胞对内皮细胞的粘附在动脉样硬化发展中至关重要.
- 雄激素可能在促进这种粘附过程中发挥作用.
研究的目的:
- 为了研究二测试 (DHT) 对单细胞对内皮细胞的粘附的影响.
- 检查DHT对内皮细胞表面粘附分子的影响.
- 为了确定雄激素受体阻断是否影响DHT诱导的单细胞粘附.
主要方法:
- 人类静脉内皮细胞 (HUVEC) 用DHT和/或氧胺 (HF) 进行治疗.
- 通过光显微镜测量单细胞对HUVECs的附着性.
- 使用ELISA量化了内皮细胞表面粘附分子表达 (VCAM-1).
主要成果:
- DHT显著增加了单细胞对HUVECs的粘附,以剂量依赖的方式.
- DHT提高了血管细胞粘附分子-1 (VCAM-1) 在内皮细胞上的表达.
- 氧胺 (HF) 阻断了增强的粘附和VCAM-1表达,反VCAM-1抗体也是如此.
结论:
- 暴露于雄激素会促进单细胞对内皮细胞的粘附.
- 这种益风性效应在一定程度上是由增加的VCAM-1表达介导的.
- 向雄激素通路或VCAM-1可能为动脉样硬化提供治疗策略.
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