© 1995 American Heart Association, Inc.
Articles |
Relative Contributions of Apolipoprotein(a) and Apolipoprotein-B to the Development of Fatty Lesions in the Proximal Aorta of Mice
From the Departments of Internal Medicine and Molecular Genetics (F.P.M., V.M., H.H.H.) and The Howard Hughes Medical Center and Department of Biochemistry (R.E.H.), University of Texas Southwestern Medical Center, Dallas; The Gladstone Institute of Cardiovascular Disease (D.L.N., J.M., S.G.Y., D.A.S.), University of California at San Francisco; and Northwest Lipid Research Laboratory (S.M.), University of Washington, Seattle.
Correspondence to Helen H. Hobbs, MD, Department of Molecular Genetics, UT Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75235-9046.
Abstract Transgenic mice expressing transgenes for both human apolipoprotein B-100 (h-apoB) and apolipoprotein(a) [apo(a)] were fed a high-fat, atherogenic diet for 14 weeks to examine the effect of lipoprotein(a) [Lp(a)] on the development of aortic fatty lesions. The extent of lesions in the proximal region of the aorta of Lp(a) mice was measured by use of a computer-assisted image analysis of 20 sections per animal and compared with that of nontransgenic mice as well as mice expressing either the apo(a) or h-apoB transgene. The control (n=23) and apo(a) (n=22) transgenic mice had very small mean lesion areas (607 versus 128 µm2 per section). The h-apoB–expressing mice (n=20) had significantly higher mean lesion areas (3288 µm2 per section) than either the control or apo(a) transgenic animals. Coexpression of apo(a) and h-apoB transgenes resulted in only a modest increase in lesion area (4678 µm2 per section, n=19). Thus, the expression of human apo(a) in C57BL/6/SJL hybrid mice fed an atherogenic diet failed to significantly potentiate the development of aortic fatty lesions in the absence or presence of high levels of h-apoB.
Key Words: apo(a) • lipoprotein(a) • transgenic mice • atherosclerosis
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