Protein kinase C and mitogen-activated protein kinase signalling in oligodendrocytes

Authors

  • Rochelle L. Stariha,

    1. Department of Medicine, Division of Neurology, UBC Hospital, University of British Columbia, Vancouver, B.C., V6T 2B5 Canada
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  • Seung U. Kim

    Corresponding author
    1. Department of Medicine, Division of Neurology, UBC Hospital, University of British Columbia, Vancouver, B.C., V6T 2B5 Canada
    • Department of Medicine, Division of Neurology, UBC Hospital, University of British Columbia, 2211 Westbrook Mall, Vancouver, B.C., V6T 2B5 Canada
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Abstract

Oligodendrocytes (OL) play a significant physiological role in the central nervous system by creating the myelin sheath that allows for the efficient conduction of nerve impulses. Therefore, it is important to understand which signalling cascades define the proliferation, differentiation, survival, and myelin formation potential of these cells. Currently, much of the knowledge in this field has focused on two sets of protein kinase signalling molecules: Protein kinase C (PKC) and the mitogen-activated protein kinases (MAPKs). The roles of these kinases in OL are complex, and appear to be highly dependent on the developmental stage of the OL. Even so, some broad conclusions can be drawn from the multitude of experiments conducted on the roles of PKC and MAPKs in OL. For instance, PKC appears to have a proliferative effect on immature OL, while at the same time having an inhibitory effect on OL differentiation. In mature OL, the effects of PKC include increased process extension and myelin formation. The extracellular signal-regulated (ERK) members of the MAPK family also appear to increase process extensions in mature OL. On the other hand, the c-Jun N-terminal kinase (JNK) and p38 kinase members of the MAPK family appear to regulate apoptotic events in OL. Microsc. Res. Tech. 52:680–688, 2001. © 2001 Wiley-Liss, Inc.

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