J. Lipid Res.
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Papers In Press, published online ahead of print January 16, 2005
J. Lipid Res., doi:10.1194/jlr.M400467-JLR200
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Submitted on November 23, 2004
Revised on January 3, 2005
Accepted on January 4, 2005

High-level lipoprotein(a) expression in transgenic mice: evidence for oxidized phospholipids in lipoprotein(a) but not in low density lipoproteins

Matthias Schneider, Joseph L. Witztum, Stephen G. Young, Erwin H. Ludwig, Elizabeth R. Miller, Sotirios Tsimikas, Linda K. Curtiss, Santica M. Marcovina, John M. Taylor, Richard M. Lawn, Thomas L. Innerarity, and Robert E. Pitas

Gladstone Institute of Cardiovascular Disease, University of California at San Francisco, San Francisco, CA 94158

Corresponding Author: rpitas{at}gladstone.ucsf.edu

Efforts to elucidate the role of lipoprotein(a) [Lp(a)] in atherogenesis have been hampered by the lack of an animal model with high plasma Lp(a) levels. We produced two lines of transgenic mice expressing apo(a) in the liver and crossed them with mice expressing human apoB-100, generating two lines of Lp(a) mice. One had Lp(a) levels of ~700 mg/dl, well above the 30 mg/dl threshold associated with increased risk of atherosclerosis in humans; the other had ~35 mg/dl. Most of the LDL in mice with high-level apo(a) expression was covalently bound to apo(a), but most of the LDL in the low-expressing line was free. Using an enzyme-linked sandwich assay with monoclonal antibody EO6, we found high levels of oxidized phospholipids in Lp(a) from high-expressing mice, but not in Lp(a) or LDL from low-expressing mice or in LDL from human apoB-100 transgenic mice (p < 0.00001), even though all mice had similar plasma levels of human apoB-100. The increase in oxidized lipids specific to Lp(a) in high level apo(a)-expressing mice suggests a mechanism by which elevated circulating levels of Lp(a) could contribute to atherogenesis.


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