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通过关闭肝脏脂蛋白分泌来消除小鼠的动脉生成
Hsiao D Lieu1, Shannon K Withycombe, Quinn Walker
1Gladstone Institute of Cardiovascular Disease, San Francisco, CA 94141-9100, USA. hlieu@gladstone.ucsf.edu
Circulation
|March 12, 2003
概括
研究人员开发了"反向小鼠",可以通过遗传关闭肝脏脂蛋白生产来逆转高胆固醇血清症并预防动脉样硬化. 这种基因开关为管理胆固醇水平和相关心血管疾病提供了一种新的方法.
科学领域:
- 心血管生物学 心血管生物学
- 遗传学 是一个遗传学.
- 代谢疾病 代谢疾病
背景情况:
- 缺乏LDL受体的小鼠 (Ldlr-/-Apob100/100) 显示高的LDL胆固醇和严重的动脉动脉样硬化.
- 一个假设提出,消除肝脏脂蛋白生产可以解决高胆固醇和动脉样硬化易感性.
研究的目的:
- 调查遗传抑制肝脂蛋白产生的潜力,以逆转高胆固醇血症和预防动脉样硬化.
- 开发一种新的小鼠模型来研究这些条件的逆转.
主要方法:
- 通过培育具有条件Mttp等位基因和Mx1-Cre转基因的Ldlr-/-Apob100/100小鼠,开发出"反向小鼠".
- 诱导肝脏中的Cre表达,以暂时消除微体甘油三转移蛋白 (Mttp) 表达和肝脏脂蛋白分泌.
- 监测血胆固醇水平和动脉样硬化的发展,以应对CRE诱导.
主要成果:
- 过渡性肝脏Cre诱导几乎消除了肝脏Mttp表达,并废除了肝脏脂蛋白分泌.
- 血LDL胆固醇水平在食小鼠 (233.9至37.2毫克/分升) 和高脂肪食小鼠 (525.7至100.6毫克/分升) 均显著下降.
- 在CRE诱导后,观察到完全预防动脉样硬化发展和相关的基因表达变化.
结论:
- 成功开发了一种小鼠模型 ("反向小鼠"),其中高胆固醇血症通过遗传开关是可逆的.
- 这些小鼠为研究高胆固醇血和动脉样硬化逆转过程中的基因表达变化提供了宝贵的工具.
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