It has also been proposed that PPARδ attenuates SCI by promoting oligodendrocyte precursor cell (OPC) proliferation and differentiation following injury. Studies have shown that OPCs accumulate at SCI sites, likely as an attempt to regenerate the damaged axons [89]. Following SCI in rats, PPARδ positive cells increased in the white matter along the lesion border for up to two weeks. Double-labeling experiments indicated there was an increase in PPARδ in NG2 positive cells, potential OPCs, and PPARδ positive CC1 cells, oligodendrocytes [90]. Given the temporal and spatial expression of PPARδ after SCI, it is possible that it can regulate oligodendrogenesis after injury.
