Not all mitogens are the same

Cambridge, UK -

Neurons communicate with each other by exchanging electrical signals through axons, or otherwise called nerve fibers. These axons are insulated by the phospholipid myelin, which acts as an insulator. Myelin is deposited on neurons of the peripheral nervous system by Schwann cells, and on neurons of the central nervous system by oligodendrocytes. Both Schwann cells and oligodendrocytes are collectively termed "glial cells".

In the study of regenerative medicine, one major area of interest is repairing neurological diseases such as multiple sclerosis, which is caused by immune-mediated loss of myelin. Particularly, the use of stem cells for remyelination has been previously described.

One main question is whether stem cells themselves differentiate into oligodendrocytes which then are capable of inducing remyelination, or whether the stem cells secrete growth factors that trigger endogenous oligodendrocytes to remyelinate nerves.

In a recent study (Wang Z et al. Contrasting effects of mitogenic growth factors on myelination in neuron-oligodendrocyte co-cultures. Glia. 2007 Jan 18) it was demonstrated that not all growth factors are actually capable of stimulating remyelination, and that some actually inhibit it.

The scientists used an interesting in vitro model system in which neurons where co-cultured with oligodendrocyte precursors. In this experimental system, the oligodendrocyte precursors are capable of inducing remyelination within, on average 14 days. While the growth factor neuregulin was capable of increasing remyelination, the two stem cell associated growth factors FGF-2 and PDGF-1 actually inhibited myelination.

This study is of great interest to stem cell therapists since it suggests that not all growth factors positively influence myelination. Specifically, it is of interest to examine these findings in light of papers like Ruffini et al (Fibroblast growth factor-II gene therapy reverts the clinical course and the pathological signs of chronic experimental autoimmune encephalomyelitis in C57BL/6 mice. Gene Ther. 2001 Aug;8(16):1207-13) which suggest that FGF-2 administration by gene therapy can actually prevent clinical onset of the mouse model of multiple sclerosis EAE.

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