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

Hsin-Lin Cheng; Michael Shy; Eva L Feldman

doi:10.1210/endo.140.10.7051

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

Journal article

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Peer reviewed

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

Hsin-Lin Cheng, Michael Shy and Eva L Feldman

Endocrinology (Philadelphia), Vol.140(10), pp.4478-4485

10/01/1999

DOI: 10.1210/endo.140.10.7051

PMID: 10499501

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Abstract

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.

Details

Title: Subtitle: Regulation of Insulin-Like Growth Factor-Binding Protein-5 Expression during Schwann Cell Differentiation1
Creators: Hsin-Lin Cheng - Department of Neurology, University of Michigan, Ann Arbor, Michigan 48109
Michael Shy - The Department of Neurology, Wayne State University (M.S.), Detroit Michigan 48201
Eva L Feldman - Department of Neurology, University of Michigan, Ann Arbor, Michigan 48109
Resource Type: Journal article
Publication Details: Endocrinology (Philadelphia), Vol.140(10), pp.4478-4485
DOI: 10.1210/endo.140.10.7051
PMID: 10499501
NLM abbreviation: Endocrinology
ISSN: 0013-7227
eISSN: 1945-7170
Language: English
Date published: 10/01/1999
Academic Unit: Neurology; Molecular Physiology and Biophysics; Stead Family Department of Pediatrics; Iowa Neuroscience Institute
Record Identifier: 9984015918402771

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