Moyon S, Dubessy AL, Aigrot MS, Trotter M, Huang JK, Dauphinot L, Potier MC, Kerninon C, Melik Parsadaniantz S, Franklin RJ, Lubetzki C. Demyelination causes adult CNS progenitors to revert to an immature state and express immune cues that support their migration.J Neurosci. 2015 Jan 7;35(1):4-20. doi: 10.1523/JNEUROSCI.0849-14.2015
The declining efficiency of myelin regeneration in individuals with multiple sclerosis has stimulated a search for ways by which it might be therapeutically enhanced. Here we have used gene expression profiling on purified mouse oligodendrocyte progenitor cells (OPCs), the remyelinating cells of the adult CNS, to obtain a comprehensive picture of how they become activated after demyelination and how this enables them to contribute to remyelination. We find that adult OPCs have a transcriptome more similar to that of oligodendrocytes than to neonatal OPCs, but revert to a neonatal-like transcriptome when activated. Part of the activation response involves increased expression of two genes of the innate immune system, IL1β and CCL2 (Macrophage chemotactic protein), which enhance the mobilization of OPCs. Our results add a new dimension to the role of the innate immune system in CNS regeneration, revealing how OPCs themselves contribute to the post-injury inflammatory milieu by producing cytokines that directly enhance their repopulation of areas of demyelination and hence their ability to contribute to remyelination.
You can all read the conclusions, is this how transplanted stem cells work. They produce factors to promote repair.This is why they can be long since gone and repair occurs when stem cellsare used, but maybe we only need to supply the factors not the stem cells.