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A role for the MAPK/ERK pathway in oligodendroglial differentiation in vitro : stage specific effects on cell branching
Author(s) -
YounesRapozo V.,
Felgueiras L.O.R.,
Via.L.,
Fierro I.M.,
BarjaFidalgo C.,
Manhães A.C.,
Barradas P.C.
Publication year - 2009
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2009.08.014
Subject(s) - mapk/erk pathway , myelin basic protein , microbiology and biotechnology , biology , oligodendrocyte , protein kinase a , kinase , myelin , oligodendroglial tumor , cellular differentiation , extracellular , biochemistry , cancer research , neuroscience , gene , central nervous system , astrocytoma , glioblastoma , oligodendroglioma
The mitogen‐activated protein kinase/extracellular signal‐regulated kinase (MAPK/ERK) pathway is important for both long‐term survival and timing of the progression of oligodendrocyte differentiation. Oligodendroglial cells treated with MEK inhibitor were distinguished by using stage specific markers: NG2 proteoglycan, A2B5, 2′3′nucleotide‐cyclic 3′phosphodiesterase (CNPase) and myelin basic protein (MBP), and classified according to their morphology into different developmental stages. Treatment significantly increased the number of cells with more immature morphologies and decreased the number of mature cells. Furthermore, it increased the number of rounded cells that could not be classified into any of the oligodendroglial developmental stages. The strongest effects were usually observed shortly after treatment. Rounded cells were CNPase/MBP positive and they were not stained by anti‐NG2 or A2B5, indicating that they were mature cells unable either to extend and/or to maintain their processes. These data showed an effect of the MAPK/ERK pathway on oligodendroglial branching, with possible consequences for the formation of the myelin sheath.