雌激素在体外和体外调节AT1受体基因表达
G Nickenig1, A T Bäumer, C Grohè
1Klinik III für Innere Medizin, Universität zu Köln, Germany. georg.nickenig@uni-koeln.de
Circulation
|June 19, 1998
概括
雌激素缺乏会增加AT1受体表达,导致高血压和动脉样硬化. 雌激素替代疗法可以逆转这种效应,强调其在心血管健康方面的保护作用.
科学领域:
- 心血管生物学 心血管生物学
- 内分泌学 在内分泌学.
- 分子医学是分子医学.
背景情况:
- 血管激素II型1 (AT1) 受体与高血压和动脉样硬化有关.
- 雌激素缺乏与心血管疾病风险增加有关.
研究的目的:
- 为了研究雌激素缺乏和替代对AT1受体基因表达在卵巢切除的老鼠的影响.
- 为了确定雌激素对血管光滑肌细胞中AT1受体表达的影响.
主要方法:
- 研究了带有和没有雌激素替代的卵巢切除的老鼠.
- 评估了 ангиотензин II诱导的血管收缩,AT1受体mRNA水平 (qPCR,北方斑块) 和AT1受体密度 (放射性体结合).
- 实验还在培养的血管光滑肌细胞中进行.
主要成果:
- 雌激素缺乏症显著增加了AT1受体密度 (160%) 和mRNA水平 (187%) 在老鼠的大脑中.
- 雌激素替代疗法使AT1受体过度表达正常化.
- 雌激素降低了AT1受体mRNA和培养血管光滑肌细胞中的密度.
结论:
- 雌激素缺乏会提高AT1受体表达的调节,这可能解释了其与高血压和动脉样硬化相关性.
- 雌激素对血管光滑肌细胞中的AT1受体表达有直接的抑制作用.
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