Insulin-like growth factor-I is necessary for neural stem cell proliferation and demonstrates distinct actions of epidermal growth factor and fibroblast growth factor-2

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Serval ID
serval:BIB_755860E86E1F
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Insulin-like growth factor-I is necessary for neural stem cell proliferation and demonstrates distinct actions of epidermal growth factor and fibroblast growth factor-2
Journal
Journal of Neuroscience
Author(s)
Arsenijevic  Y., Weiss  S., Schneider  B., Aebischer  P.
ISSN
1529-2401 (Electronic)
Publication state
Published
Issued date
09/2001
Volume
21
Number
18
Pages
7194-202
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Sep 15
Abstract
Neural stem cells (NSCs), when stimulated with epidermal growth factor (EGF) or fibroblast growth factor-2 (FGF-2), have the capacity to renew, expand, and produce precursors for neurons, astrocytes, and oligodendrocytes. We postulated that the early appearance of insulin-like growth factor (IGF-I) receptors during mouse striatum development implies a role in NSC regulation. Thus, we tested in vitro the action of IGF-I on the proliferation of striatal NSCs. In the absence of IGF-I, neither EGF nor FGF-2 was able to induce the proliferation of E14 mouse striatal cells. However, addition of IGF-I generated large proliferative clusters, termed spheres, in a dose-dependent manner. The newly generated spheres were multipotent, and clonal analysis revealed that EGF or FGF-2, in the presence of IGF-I, acted directly on NSCs. The actions of IGF-I suggest distinct modes of action of EGF or FGF-2 on NSCs. First, continuous versus delayed administration of these neurotrophic factors showed that neither IGF-I nor EGF had an effect on NSC survival, whereas FGF-2 promoted the survival or maintenance of the stem cell state of 50% of NSCs for 6 d. Second, short-term exposure to IGF-I induced the proliferation of NSCs in the presence of EGF, but not of FGF-2, through an autocrine secretion of IGF-I. These findings suggest that IGF-I is a key factor in the regulation of NSC activation and that EGF and FGF-2 control striatal NSC proliferation, in part, through distinct intracellular mechanisms.
Keywords
Animals Autocrine Communication/drug effects/physiology Cell Count Cell Division/drug effects Cell Survival/drug effects Cells, Cultured Corpus Striatum Dose-Response Relationship, Drug Epidermal Growth Factor/*pharmacology Fibroblast Growth Factor 2/*pharmacology Insulin-Like Growth Factor I/*pharmacology Mice Neurons/cytology/*drug effects/metabolism Spheroids, Cellular/cytology/drug effects Stem Cells/cytology/*drug effects/metabolism
Pubmed
Web of science
Create date
28/01/2008 12:31
Last modification date
20/08/2019 14:32
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