Insulin-like growth factor-I is a differentiation factor for postmitotic CNS stem cell-derived neuronal precursors: distinct actions from those of brain-derived neurotrophic factor.

Détails

ID Serval
serval:BIB_8C832AFA7026
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Insulin-like growth factor-I is a differentiation factor for postmitotic CNS stem cell-derived neuronal precursors: distinct actions from those of brain-derived neurotrophic factor.
Périodique
Journal of Neuroscience
Auteur(s)
Arsenijevic Y., Weiss S.
ISSN
0270-6474 (Print)
ISSN-L
0270-6474
Statut éditorial
Publié
Date de publication
03/1998
Volume
18
Numéro
6
Pages
2118-2128
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review
WOS Document Type: Article
Résumé
Insulin-like growth factor-I (IGF-I) has been reported previously to promote the proliferation, survival, and maturation of sympathetic neuroblasts, the genesis of retinal neurons, and the survival of CNS projection and motor neurons. Here we asked whether IGF-I could promote the in vitro differentiation of postmitotic mammalian CNS neuronal precursors derived from multipotent epidermal growth factor (EGF)-responsive stem cells. In the absence of IGF-I, virtually no neurons were present in cultured stem cell progeny, whereas IGF-I increased neuron number by eight- to 40-fold. Brief exposures (2 hr) to IGF-I were sufficient to allow for neuronal differentiation without affecting proliferation or survival. IGF-I actions could be mimicked by insulin and IGF-II at concentrations that correspond to the pharmacology of the IGF-I receptor, the latter for which the mRNA was detected in undifferentiated stem cell progeny. Although ineffectual alone at low concentrations (10 nM) that would activate its own receptor, insulin was able to potentiate the actions of IGF-I by acting on mitotically active neural precursors. When neuronal precursor differentiation by IGF-I was examined in relation to brain-derived neurotrophic factor (BDNF), two important observations were made: (1) BDNF could potentiate the differentiating actions of IGF-I plus insulin, and (2) BDNF could act on a separate population of precursors that did not require IGF-I plus insulin for differentiation. Taken together, these results suggest that IGF-I and BDNF may act together or sequentially to promote neuronal precursor differentiation.
Mots-clé
Animals, Brain/cytology, Brain/physiology, Brain-Derived Neurotrophic Factor/pharmacology, Brain-Derived Neurotrophic Factor/physiology, Cell Count/drug effects, Cell Differentiation/physiology, Drug Synergism, Insulin/pharmacology, Insulin-Like Growth Factor I/metabolism, Insulin-Like Growth Factor I/pharmacology, Mice/embryology, Mitosis/physiology, Neurons/cytology, Neurons/physiology, Receptors, Somatomedin/physiology, Stem Cells/cytology, Stem Cells/drug effects
Pubmed
Web of science
Création de la notice
28/01/2008 13:31
Dernière modification de la notice
03/03/2018 19:13
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