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Intracellular events mediating insulin‐like growth factor I‐induced oligodendrocyte development: modulation by cyclic AMP
Author(s) -
Palacios Nuria,
SánchezFranco Franco,
Fernández Miriam,
Sánchez Isabel,
Cacicedo Lucinda
Publication year - 2005
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2005.03419.x
Subject(s) - oligodendrocyte , mapk/erk pathway , microbiology and biotechnology , intracellular , protein kinase a , biology , insulin like growth factor , phosphatidylinositol , signal transduction , kinase , growth factor , endocrinology , biochemistry , myelin , receptor , central nervous system
Insulin‐like growth factor I (IGF‐I) is a potent inducer of oligodendrocyte development and myelination. Although IGF‐I intracellular signaling has been well described in several cell types, intracellular mechanisms for IGF‐I‐induced oligodendrocyte development have not been defined. By using specific inhibitors of intracellular signaling pathways, we report here that the MAPK and phosphatidylinositol 3‐kinase signaling pathways are required for the full effect of IGF‐I on oligodendrocyte development in primary mixed rat cerebrocortical cell cultures. The MAPK activation, but not the phosphatidylinositol 3‐kinase activation, leads to phosphorylation of the cAMP response element‐binding protein, which is necessary for IGF‐I to induce oligodendrocyte development. cAMP, although it does not show any effect on oligodendrocyte development, has an inhibitory effect on IGF‐I‐induced oligodendrocyte development that is mediated by the cAMP‐dependent protein kinase. Furthermore, cAMP also has an inhibitory effect on IGF‐I‐dependent MAPK activation. This is a cAMP‐dependent protein kinase‐independent effect and probably contributes to the cAMP action on IGF‐I‐induced oligodendrocyte development.