Factor V Leiden mutation leads to enhanced atherosderosis in apolipoprotein E deficient mice
10.3760/cma.j.issn.0253-3758.2009.01.013
- VernacularTitle:凝血因子V莱顿突变对载脂蛋白E基因敲除小鼠动脉粥样硬化的影响
- Author:
Yue-Chun SHEN
1
;
Dong-Feng LU
;
Jun WU
;
Jie-Zhen PAN
;
Chao-Chen ZHAO
;
De-Xi HU
;
Jun LI
Author Information
1. 广州医学院附属第一医院
- Keywords:
Atheroscleroeis: Fibrin;
Heredity
- From:
Chinese Journal of Cardiology
2009;37(1):59-62
- CountryChina
- Language:Chinese
-
Abstract:
Objective Factor V Leiden(FvL)causing activated protein C resistance is a genetic risk factor for venous thrombosis in humans,and it's effect on atherosclemsis is controversial.We evaluated the effect of FvL mutation on atherosclerosis in apolipoprotein E deftcient mice fed with normal diet.Methods Degree of atherosclerosis and tissue fibrin deposition were determined in Fv+/+ApoE-/-,FvQ/ApoE-/-and FvQ/QApoE-/-mice.Results In the presence of ApoE deficiency.homozygous FvL significandy increased atherosclerosis coverage in ApoE-/-mice(FvQ/QApoE-/-vs.Fv+/+ApoE-/-=5.0%±1.1%vs.2.2%±0.4%,P＜0.005)and tissue fibrin deposition in atherosclerotic lesion(FvQ/QApoE-/-vs.Fv+/ApoE-/-=3.4%±0.5%vs.1.8%±0.4%,P＜0.05).The atherosclerotic Iesion of FvQ/+ApoE-/-mice was intermediate between FvQ/Q ApoE -/-and Fv+/ApoE-/-,and there was no significant difference comparing with any of them.Condusions Therie observations demonstrate that homozygous FvL could promote atherosclerosis and fibrin deposition in apolipoprotein E deficient mice suggesting that Factor V mutation could be an important genetic risk factor for the enhanced atherosclerosis in human.
