Atherosclerosis and Lipoproteins |
From the Department of Radiology and Cardiovascular Research Center (W.S.), University of Virginia, Charlottesville, and the Department of Medicine and Department of Microbiology and Molecular Genetics (W.S., X.W., K.T., J.W., Y.S., A.J.L.), University of California, Los Angeles.
Correspondence to Aldons J. Lusis, Department of Medicine, UCLA, 47-123 CHS, Los Angeles, CA 90095-1679. E-mail jlusis{at}mednet.ucla.edu
Previous studies showed that reconstitution of atherosclerosis-susceptible C57BL/6 (B6) female mice with apolipoprotein E (apoE)-deficient (apoE-/-) bone marrow resulted in markedly increased atherosclerosis, despite the fact that plasma lipid levels were unchanged. To determine whether apoE-/- bone marrow would increase atherosclerosis in an atherosclerosis-resistant strain, female C3H/HeJ (C3H) mice were lethally irradiated and reconstituted with bone marrow from either C3H.apoE-/- mice or wild-type C3H mice. Four weeks after transplantation, the mice were fed an atherogenic diet for 12 weeks. We found that reconstitution of C3H mice with apoE-/- bone marrow resulted in a slight reduction in plasma apoE levels and a dramatic reduction in apoE and apolipoprotein B (apoB) in the aortic wall. Plasma apoB and cholesterol levels were unchanged, as were atherosclerotic lesions at the aortic root. These data indicate that reconstitution of C3H mice with apoE-/- bone marrow has no effect on atherosclerosis susceptibility and that apoE promotes accumulation of apoB in the vessel wall.
Key Words: atherosclerosis macrophages bone marrow transplantation apolipoprotein E mice
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