[Factor V Leiden mutation leads to enhanced atherosclerosis in apolipoprotein E deficient mice].
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 atherosclerosis is controversial. We evaluated the effect of FvL mutation on atherosclerosis in apolipoprotein E deficient 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 significantly 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 lesion of FvQ/+ApoE-/- mice was intermediate between FvQ/Q ApoE-/- and Fv+/+ApoE-/-, and there was no significant difference comparing with any of them.


CONCLUSIONS
These 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.
Shen
Yue-chun
YC
Department of Cardiology, First Affiliated Hospital, Guangzhou Medical College, Guangzhou 510120, China.
Lu
Dong-feng
DF
Wu
Jun
J
Pan
Jie-zhen
JZ
Zhao
Chao-chen
CC
Hu
De-xi
DX
Li
Jun
J
D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics*; D050197:Atherosclerosis / Q000235:genetics*; D005165:Factor V / Q000235:genetics*; D005838:Genotype; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009154:Mutation; D010641:Phenotype
D001057:Apolipoproteins E; C095381:factor V Leiden; D005165:Factor V