PDGF is the most potent proliferative factor for OPCs, and the effect of golli on OPC proliferation occurs only in the presence of growth factors.
The present study has not only underscored the importance of golli on OPC differentiation, but also revealed separate Ca2+ signalling pathways by which OPC proliferation and death may be regulated.
These results are consistent with the known role of Shh signalling in hindbrain OPC specification, and mimics the previously described effect of disc1 knockdown on OPC development.
Although beyond the scope of this study to determine the exact composition and stoichiometry of OL KATP channels, the observed effects of the different KATP channel activators on OPC proliferation supports the presence of SUR2A/B and Kir6.1/Kir6.2, subunits in OPCs.
PDGFα is the archetypal chemoattractant for OPCs, although it is difficult to separate this effect from its effect on OPC proliferation.
Indeed, the authors provide evidence that one such inhibitor can counteract the detrimental effects of fibrinogen on OPC differentiation, pointing to a possible avenue for therapy.
To evaluate the effects of RNS60 on OPC differentiation we considered both early and late stages of differentiation under optimal conditions with and without RNS60.
For differentiation, demyelination was induced by LPC injection after the last tamoxifen injection and mice were sacrificed 10 days after to evaluate the effect on OPC differentiation.
This interpretation was further supported by the similar effect of HDAC inhibitors and PRMT5 inhibitors on OPC differentiation and by the rescue of differentiation using KAT inhibitors.
Studies based on OPC have been shown to work well; many different valve models have gained FDA market approval based on this methodology.
Writing in Neuron, Petersen et al.1 report that a blood-coagulation factor called fibrinogen (which enters the brain when the blood brain barrier is damaged in MS2) puts a brake on OPC differentiation.
