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对V因子Leiden的同卵性导致小鼠增强的血栓形成和动脉样硬化
Daniel T Eitzman1, Randal J Westrick, Yuechun Shen
1Division of Cardiology, University of Michigan Medical Center, Ann Arbor 48109-0644, USA. deitzman@umich.edu
Circulation
|April 6, 2005
概括
在小鼠中,因子V莱登 (FVL) 均性加速了动脉血栓形成和动脉样硬化. 这种效应源于循环中的非血小板衍生的血FVL,而不是来自骨髓细胞.
科学领域:
- 血管生物学 血管生物学
- 血栓形成研究研究
- 心血管疾病的遗传学
背景情况:
- 由于因子V莱登 (FVL) 的激活蛋白C抵抗是已知的静脉血栓形成的危险因素.
- 在动脉血栓塞和动脉样硬化中FVL的作用仍然存在争议.
研究的目的:
- 在小鼠模型中研究FVL突变对动脉血栓形成的影响.
- 确定FVL对动脉样硬化发展的贡献.
主要方法:
- 光化学性动脉损伤被用于诱导野生型,异合体和同合体FVL小鼠的血栓形成.
- 进行了骨髓移植实验,以确定FVL效应的来源.
- 缺乏FVL的小鼠与缺乏ApoE的小鼠交叉,以评估动脉样硬化.
主要成果:
- 与野生类型小鼠相比,同卵性FVL小鼠的闭塞性血栓形成时间显著缩短.
- 骨髓移植显示,循环血FVL,而不是骨髓衍生细胞,加速了血栓形成.
- 在ApoE缺乏的小鼠中,FVL同性加剧了大动脉动脉样硬化.
结论:
- 对于FVL突变的同胞性在小鼠中促进动脉血栓形成和动脉样硬化.
- FVL的促血栓和促动脉样硬化作用是由循环的血因子介导的,而不是骨髓衍生细胞.
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