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Originally published In Press as doi:10.1074/jbc.M910419199 on March 15, 2000

J. Biol. Chem., Vol. 275, Issue 21, 16360-16365, May 26, 2000
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Nerve Growth Factor Protects Oligodendrocytes from Tumor Necrosis Factor-alpha -induced Injury through Akt-mediated Signaling Mechanisms*

Riya TakanoDagger §, Shin HisaharaDagger ||, Kazuhiko Namikawa**, Hiroshi Kiyama**, Hideyuki OkanoDagger Dagger Dagger , and Masayuki MiuraDagger Dagger Dagger §§

From the Dagger  Division of Neuroanatomy and Dagger Dagger  Core Research for Evolutional Science and Technology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan, the § Department of Molecular Genetics, Institute of Development, Aging, and Cancer, Tohoku University, Sendai 980-8575, Japan, and the ** Department of Anatomy, Asahikawa Medical College, Asahikawa 078-8510, Japan

Tumor necrosis factor-alpha is thought to be one of the most important inflammatory cytokines associated with the demyelinating disease multiple sclerosis. We determined whether neurotrophins could protect oligodendrocytes from tumor necrosis factor-alpha -mediated cytotoxicity. Among the neurotrophins tested, nerve growth factor was most effective at preventing cell death. Nerve growth factor also prevented the tumor necrosis factor-induced loss of mitochondrial membrane potential. Overexpression of constitutively active Akt, a downstream target of phosphatidylinositol 3-kinase, but not of constitutively active MEK, protected oligodendrocytes from tumor necrosis factor-induced injury. Moreover, overexpression of dominant-negative Akt negated the protective effects of nerve growth factor on tumor necrosis factor-mediated oligodendrocyte cytotoxicity. These findings indicate that the Akt pathway is crucial in nerve growth factor-mediated oligodendrocyte protection.

* This work was supported by grants (to H. O.) from the Human Frontier Science Program and from Core Research for Evolutional Science and Technology, Japan Science and Technology Corp., and by grants-in-aid (to M. M. and H. O.) from the Ministry of Education, Science, and Culture of Japan.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: Lab. for Molecular Neurogenesis, Brain Science Institute, RIKEN, Saitama 351-0198, Japan.

|| Research Fellow of the Japan Society for the Promotion of Science.

§§ To whom correspondence should be addressed: Div. of Neuroanatomy (D12), Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. Tel.: 81-6-6879-3581; Tax: 81-6-6879-3589; E-mail: mmiura@nana.med.osaka-u.ac.jp.

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