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Originally published In Press as doi:10.1074/jbc.M000602200 on August 11, 2000

J. Biol. Chem., Vol. 275, Issue 43, 33974-33980, October 27, 2000
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Apolipoprotein E Receptors Mediate the Effects of beta -Amyloid on Astrocyte Cultures*

Mary Jo LaDuDagger , Javeed Ali Shah§, Catherine A. Reardon§, Godfrey S. Getz§, Guojun Bu, Jingru Hu||, Ling Guo||, and Linda J. Van Eldik||**Dagger Dagger

From the Dagger  Department of Medicine, Evanston Northwestern Healthcare Research Institute, Evanston, Illinois 60201, the § Department of Pathology, University of Chicago, Chicago, Illinois 60637, the  Department of Pediatrics and the Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110, and the || Department of Cell and Molecular Biology and ** Northwestern Drug Discovery Program, Northwestern University Medical School, Chicago, Illinois 60611

We have previously shown that beta -amyloid (Abeta ) induces astrocyte activation in vitro and that this reaction is attenuated by the addition of exogenous apolipoprotein E (apoE)-containing particles. However, the effects of Abeta on endogenous apoE and apoJ levels and the potential role of apoE receptors in astrocyte activation have not been addressed. Three activating stimuli (lipopolysaccharide, dibutyryl cAMP, and aged Abeta 1-42) were used to induce activation of rat astrocyte cultures, as assessed by changes in morphology and an increase in interleukin-1beta . However, only Abeta also induced ~50% reduction in the amount of released apoE and apoJ and an 8-fold increase in the levels of cell-associated apoE and apoJ. Experiments using two concentrations of receptor-associated protein, an inhibitor of apoE receptors with a differential affinity for the low density lipoprotein receptor (LDLR) and the LDLR-related protein (LRP), suggest that LRP mediates Abeta -induced astrocyte activation, whereas LDLR mediates the Abeta -induced changes in apoE levels. Receptor-associated protein had no effect on apoJ levels or on activation by either dibutyryl cAMP or lipopolysaccharide. These data suggest that apoE receptors translate the presence of extracellular Abeta into cellular responses, both initiating and modulating the inflammatory response induced by Abeta .

* This work was supported in part by National Institutes of Health Grants AG16776 (to M. J. L. D.), AG13939 (to L. V. E.), AG15501 (to L. V. E.), and NS37525 (to G. B.), a Brain Research Foundation research grant (to G. S. G.), and American Health Assistance Foundation Grant 97006 (to G. S. G.).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.

Dagger Dagger To whom correspondence should be addressed: Northwestern University Medical School, 303 E. Chicago Ave., Ward 4-202, Chicago, IL 60611-3008. Tel.: 312-503-0697; Fax: 312-503-0007; E-mail: vaneldik@northwestern.edu.

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