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Regulation of Insulin-Like Growth Factor-Binding Protein-5 Expression during Schwann Cell Differentiation¹

Department of Neurology, University of Michigan, Ann Arbor, Michigan 48109; and the Department of Neurology, Wayne State University (M.S.), Detroit Michigan 48201

Address all correspondence and requests for reprints to: Eva L. Feldman, M.D., Ph.D., Department of Neurology, University of Michigan, 200 Zina Pitcher Place, 4414 Kresge III, Ann Arbor, Michigan 48109-0588. E-mail: efeldman{at}umich.edu

We have reported that immortalized Schwann cells (SC) express the insulin-like growth factor I receptor and IGF-binding protein-5 (IGFBP-5). IGF-I promotes SC survival and protects IGFBP-5 in SC-conditioned medium from proteolysis. In the current study we examined the roles of IGF-I and IGFBP-5 in primary SC. IGF-I enhances primary SC differentiation and gene and protein expression of IGFBP-5 and the myelinating protein, P₀. SC that stably overexpress human IGFBP-5 also have higher levels of P₀ gene expression. The phosphatidylinositol-3 kinase inhibitor (LY294002), but not the mitogen-activated protein kinase kinase inhibitor (PD98059), blocks IGF-I enhancement of IGFBP-5 gene and protein expression. Collectively, these results suggest that IGF-I promotes SC differentiation, and this may occur in part by enhancing IGFBP-5 expression via phosphatidylinositol-3 kinase activation. These data support a link between enhanced IGFBP-5 expression and cellular differentiation.

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