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Research Article Free access | 10.1172/JCI118098

Treatment of severe hypercholesterolemia in apolipoprotein E-deficient mice by bone marrow transplantation.

W A Boisvert, J Spangenberg, and L K Curtiss

Department of Immunology, Scripps Research Institute, La Jolla, California 92037, USA.

Find articles by Boisvert, W. in: JCI | PubMed | Google Scholar

Department of Immunology, Scripps Research Institute, La Jolla, California 92037, USA.

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Department of Immunology, Scripps Research Institute, La Jolla, California 92037, USA.

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Published August 1, 1995 - More info

Published in Volume 96, Issue 2 on August 1, 1995
J Clin Invest. 1995;96(2):1118–1124. https://doi.org/10.1172/JCI118098.
© 1995 The American Society for Clinical Investigation
Published August 1, 1995 - Version history
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Abstract

Apo E, a key regulator of cholesterol-rich lipoprotein metabolism, is synthesized by numerous extrahepatic tissues. Although its synthesis in macrophages is documented, the contribution of macrophage-derived apo E to hepatic clearance of serum cholesterol is unknown. To address this issue bone marrow transplantation was performed on hypercholesterolemic apo E-deficient mice with either syngeneic apo E-deficient mouse bone marrow cells (E0-control) or wild-type mouse bone marrow cells expressing apo E (E0-treated). E0-control and E0-treated mice were fed either a regular chow diet or an atherogenic diet (designated E0-control-HF and E0-treated-HF). Serum cholesterol levels dropped dramatically in the E0-treated mice largely due to a reduction in their VLDL cholesterol. No changes were seen in the E0-control mice. After 4 wk serum cholesterol in E0-treated-HF mice was about four-fold lower compared to E0-control-HF animals. Moreover, the extent of atherosclerosis in the E0-treated-HF mice after 14-16 wk was greatly reduced. Wild-type apo E mRNA was detected in the liver, spleen, and brain of the E0-treated mice indicating that apo E gene transfer was successfully achieved through bone marrow transplantation. More importantly, the level of apo E expression was sufficient to reduce the severe hypercholesterolemia of the apo E-deficient mice fed either chow or atherogenic diets.

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Referenced in 1 patents
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