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  • Title: Apolipoprotein A-I deficiency results in markedly increased atherosclerosis in mice lacking the LDL receptor.
    Author: Moore RE, Kawashiri MA, Kitajima K, Secreto A, Millar JS, Pratico D, Rader DJ.
    Journal: Arterioscler Thromb Vasc Biol; 2003 Oct 01; 23(10):1914-20. PubMed ID: 12933536.
    Abstract:
    OBJECTIVE: An inverse and independent association between plasma levels of apolipoprotein (apo) A-I and coronary heart disease in humans is well established. ApoA-I is the primary protein component of HDL and is thought to play an important role in mediating several of the atheroprotective effects of HDL. However, studies of the effects of apoA-I deficiency on the development of atherosclerosis in mice have not been definitive. We examined the effects of apoA-I deficiency on plasma lipids and atherosclerosis in LDL receptor-deficient mice fed a chow diet for up to 22 months. METHODS AND RESULTS: Both apoA-I-deficient (apoA-I-/-)/LDL receptor-deficient (LDLR-/-) and LDLR-/- mice had a similar moderate elevation of non-HDL cholesterol (non-HDL-C). Unlike previous studies of apoA-I deficiency in which the HDL-C levels were extremely low, the apoA-I-/-/LDLR-/- mice in this study had substantial levels of HDL-C that were similar to wild-type mice. Despite similar levels of non-HDL-C and substantial levels of HDL-C, apoA-I-/-/LDLR-/- mice develop significantly more atherosclerosis (up to a 5-fold increase) and oxidant stress (39% increase) than LDLR-/- mice. CONCLUSIONS: These results demonstrate that despite normal levels of HDL-C, apoA-I deficiency is associated with a significant loss of protection from the formation of atherosclerosis in LDLR-/- mice fed a chow diet.
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