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Originally published In Press as doi:10.1074/jbc.M300819200 on March 7, 2003

J. Biol. Chem., Vol. 278, Issue 20, 18408-18418, May 16, 2003
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Transforming Growth Factor-beta 1 Potentiates Amyloid-beta Generation in Astrocytes and in Transgenic Mice*

Sylvain LesnéDagger **, Fabian DocagneDagger §**, Cecília GabrielDagger , Géraldine LiotDagger , Debomoy K. Lahiri, Luc Buée||, Laurent PlawinskiDagger , André Delacourte||, Eric T. MacKenzieDagger , Alain BuissonDagger **, and Denis VivienDagger **Dagger Dagger

From the Dagger  Unité Mixte de Recherche (UMR) CNRS 6551, IFR47, Université de Caen, Cyceron, Caen Cedex 14074, France,  Department of Psychiatry, Institute of Psychiatric Research, Indiana University School of Medicine, Indianapolis, Indiana 46202, and || Unité INSERM 422, Vieillissement Cérébral et Dégénérescence Neuronale, Lille Cedex 59045, France

Accumulation of the amyloid-beta peptide (Abeta ) in the brain is crucial for development of Alzheimer's disease. Expression of transforming growth factor-beta 1 (TGF-beta 1), an immunosuppressive cytokine, has been correlated in vivo with Abeta accumulation in transgenic mice and recently with Abeta clearance by activated microglia. Here, we demonstrate that TGF-beta 1 drives the production of Abeta 40/42 by astrocytes leading to Abeta production in TGF-beta 1 transgenic mice. First, TGF-beta 1 induces the overexpression of the amyloid precursor protein (APP) in astrocytes but not in neurons, involving a highly conserved TGF-beta 1-responsive element in the 5'-untranslated region (+54/+74) of the APP promoter. Second, we demonstrated an increased release of soluble APP-beta which led to TGF-beta 1-induced Abeta generation in both murine and human astrocytes. These results demonstrate that TGF-beta 1 potentiates Abeta production in human astrocytes and may enhance the formation of plaques burden in the brain of Alzheimer's disease patients.

* This work was supported to grants from the Regional Council of Lower Normandy (to S. L.), the French Ministry of Research and Technology (to G. L.), the National Center for Scientific Research CNRS (to C. G.), and the National Institutes of Health (to D. K. L.).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.

§ Present address: CNS Inflammation Group, Centre for Neuroscience at Southampton, University of Southampton, Biomedical Sciences Bldg., Southampton SO16 7PX, UK.

** These authors contributed equally to this work.

Dagger Dagger To whom correspondence should be addressed: UMR CNRS 6551, Université de Caen, Centre Cyceron, Boulevard Henri Becquerel, BP 5229, Caen Cedex 14074, France. Tel.: 33-2-3156-6039; Fax: 33-2-3156-6199; E-mail: d.vivien@neuro.unicaen.fr.

Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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