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J. Biol. Chem., Vol. 275, Issue 26, 19883-19890, June 30, 2000
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Uptake of Lipoproteins for Axonal Growth of Sympathetic Neurons*

Elena I. Posse de ChavesDagger §, Dennis E. Vance||, Robert B. Campenot||**, Robert S. Kiss, and Jean E. VanceDagger Dagger Dagger

From the Departments of  Biochemistry, ** Cell Biology, and Dagger  Medicine, University of Alberta, Edmonton, Alberta T6G 2S2, Canada

Lipoproteins originating from axon and myelin breakdown in injured peripheral nerves are believed to supply cholesterol to regenerating axons. We have used compartmented cultures of rat sympathetic neurons to investigate the utilization of lipids from lipoproteins for axon elongation. Lipids and proteins from human low density lipoproteins (LDL) and high density lipoproteins (HDL) were taken up by distal axons and transported to cell bodies, whereas cell bodies/proximal axons internalized these components from only LDL, not HDL. Consistent with these observations, the impairment of axonal growth, induced by inhibition of cholesterol synthesis, was reversed when LDL or HDL were added to distal axons or when LDL, but not HDL, were added to cell bodies. LDL receptors (LDLRs) and LR7/8B (apoER2) were present in cell bodies/proximal axons and distal axons, with LDLRs being more abundant in the former. Inhibition of cholesterol biosynthesis increased LDLR expression in cell bodies/proximal axons but not distal axons. LR11 (SorLA) was restricted to cell bodies/proximal axons and was undetectable in distal axons. Neither the LDL receptor-related protein nor the HDL receptor, SR-B1, was detected in sympathetic neurons. These studies demonstrate for the first time that lipids are taken up from lipoproteins by sympathetic neurons for use in axonal regeneration.

* This work was supported in part by grants from the Medical Research Council of Canada and the Heart and Stroke Foundation of Alberta/Northwest Territories.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Supported by postdoctoral fellowships from the Alberta Heritage Foundation for Medical Research and the Alberta Paraplegic Foundation. Present address: Dept. of Pharmacology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB T6G 2S2, Canada.

|| Medical Scientists of the Alberta Heritage Foundation for Medical Research.

Dagger Dagger To whom correspondence should be addressed: 328 Heritage Medical Research Centre, Faculty of Medicine, University of Alberta, Edmonton, Alberta T6G 2S2, Canada. Tel.: 780-492-7250; Fax: 780-492-3383; E-mail: Jean.Vance@ualberta.ca.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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