Protein kinase C and mitogen-activated protein kinase signalling in oligodendrocytes
Article first published online: 16 MAR 2001
Copyright © 2001 Wiley-Liss, Inc.
Microscopy Research and Technique
Special Issue: Oligodendrocytes
Volume 52, Issue 6, pages 680–688, 15 March 2001
How to Cite
Stariha, R. L. and Kim, S. U. (2001), Protein kinase C and mitogen-activated protein kinase signalling in oligodendrocytes. Microsc. Res. Tech., 52: 680–688. doi: 10.1002/jemt.1052
- Issue published online: 16 MAR 2001
- Article first published online: 16 MAR 2001
- Manuscript Accepted: 24 OCT 2000
- Manuscript Received: 3 AUG 2000
- process extension;
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.