Factor V Leiden mutation leads to enhanced atherosclerosis in apolipoprotein E deficient mice / 中华心血管病杂志
Chinese Journal of Cardiology
;
(12): 59-62, 2009.
Artigo
em Chinês
| WPRIM
| ID: wpr-294778
ABSTRACT
<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>Degree of atherosclerosis and tissue fibrin deposition were determined in Fv+/+ApoE-/-, FvQ/+ApoE-/- and FvQ/QApoE-/- mice.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSIONS</b>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.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Apolipoproteínas E
/
Fenótipo
/
Fator V
/
Camundongos Knockout
/
Aterosclerose
/
Genética
/
Genótipo
/
Camundongos Endogâmicos C57BL
/
Mutação
Tipo de estudo:
Fatores de risco
Limite:
Animais
Idioma:
Chinês
Revista:
Chinese Journal of Cardiology
Ano de publicação:
2009
Tipo de documento:
Artigo
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