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Originally published In Press as doi:10.1074/jbc.M002534200 on May 26, 2000

J. Biol. Chem., Vol. 275, Issue 35, 27197-27204, September 1, 2000
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GTPases and Phosphatidylinositol 3-Kinase Are Critical for Insulin-like Growth Factor-I-mediated Schwann Cell Motility*

Hsin-Lin Cheng, Matthew L. Steinway, James W. Russell, and Eva L. FeldmanDagger

From the Department of Neurology, University of Michigan, Ann Arbor, Michigan 48109

Previously, we reported insulin-like growth factor-I (IGF-I) promotes motility and focal adhesion kinase (FAK) activation in neuronal cells. In the current study, we examined the role of IGF-I in Schwann cell (SC) motility. IGF-I increases SC process extension and motility. In parallel, IGF-I activates IGF-I receptor, insulin receptor substrate-1 (IRS-1), phosphatidylinositol 3 (PI-3)-kinase, and FAK. LY294002, a PI-3 kinase inhibitor, blocks IGF-I-induced motility and FAK phosphorylation. The Rho family of GTPases is important in the regulation of the cytoskeleton. Overexpression of constitutively active Leu-61 Cdc42 and Val-12 Rac1 enhances SC motility which is unaffected by LY294002. In parallel, stable transfection of SC with dominant negative Asn-17 Rac1 blocks IGF-I-mediated SC motility and FAK phosphorylation, implying Rac is an upstream regulator of FAK. Collectively our results suggest that IGF-I regulates SC motility by reorganization of the actin cytoskeleton via the downstream activation of a PI-3 kinase, small GTPase, and FAK pathway.

* This work was supported by National Institutes of Health Grants NS01938 (to J. W. R.), NS36778, and NS38849, grants from the Juvenile Diabetes Foundation Center of Excellence for the Study of the Complications of Diabetes, the American Diabetes Association (to E. L. F.), and the Program for Understanding Neurological Diseases.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 To whom correspondence should be addressed: Dept. of Neurology, University of Michigan, 200 Zina Pitcher Place, 4414 Kresge III, Ann Arbor, MI 48109-0588. Tel.: 734-763-7274; Fax: 734-763-7275; E-mail: efeldman@umich.edu.

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