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Published 5 January 2004. doi:10.1083/jcb.200308101
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 164, Number 1, 111-122
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Article

IGF-I instructs multipotent adult neural progenitor cells to become oligodendrocytes



Jenny Hsieh1, James B. Aimone1, Brian K. Kaspar1, Tomoko Kuwabara1, Kinichi Nakashima1,2 and Fred H. Gage1

1 Laboratory of Genetics, The Salk Institute, La Jolla, CA 92037
2 Department of Cell Fate Modulation, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan

Address correspondence to Fred H. Gage, The Salk Institute, 10010 N. Torrey Pines Road, La Jolla, CA 92037. Tel.: (858) 453-4100. Fax: (858) 597-0824. email: gage{at}salk.edu

Adult multipotent neural progenitor cells can differentiate into neurons, astrocytes, and oligodendrocytes in the mammalian central nervous system, but the molecular mechanisms that control their differentiation are not yet well understood. Insulin-like growth factor I (IGF-I) can promote the differentiation of cells already committed to an oligodendroglial lineage during development. However, it is unclear whether IGF-I affects multipotent neural progenitor cells. Here, we show that IGF-I stimulates the differentiation of multipotent adult rat hippocampus-derived neural progenitor cells into oligodendrocytes. Modeling analysis indicates that the actions of IGF-I are instructive. Oligodendrocyte differentiation by IGF-I appears to be mediated through an inhibition of bone morphogenetic protein signaling. Furthermore, overexpression of IGF-I in the hippocampus leads to an increase in oligodendrocyte markers. These data demonstrate the existence of a single molecule, IGF-I, that can influence the fate choice of multipotent adult neural progenitor cells to an oligodendroglial lineage.

Key Words: glia; neural stem cell; insulin; BMP; hippocampus

Abbreviations used in this paper: AAV, adeno-associated virus; BMP, bone morphogenetic protein; CNS, central nervous system; IGF, insulin-like growth factor; MBP, myelin basic protein; RA, retinoic acid.


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