Protective effect of Lithium on Schwann cell transplantation via Wnt/β-catenin signaling pathway after spinal cord injury in vitro and vivo

Schwann cell is one of the most widely studied cell types for repair of the spinal cord. Following the spinal cord injury (SCI). For transplantation, large numbers of Schwann cells are necessary to fill injury-induced cystic cavities. Lithium chloride could exhibit neuroprotection after SCI, however, the molecular mechanism of which remains unknown. This study demonstrated that lithium chloride exhibited neuroprotective effects on survival and proliferation of cultured SCs in vitro and in vivo of a SCI model via activating the Wnt/beta-catenin signaling pathway. We constructed the Dominant-active beta-cantenin-GFP tet-off lentivirus and obtained the Wnt signaling activated SCs in vitro. Then transplanted them to explore the effect on long-term survival, proliferation and regeneration of axons in the injured spinal cord of mice. Results showed that primary cultured SCs treated with lithium chloride significantly up-regulated the expression of beta-catenin and decreased the beta-catenin phosphorylation (p-beta-catenin), improved the survival and proliferation of cultured SCs, and increased the axonal growth of dorsal root ganglion (DRG) in vitro; moreover, the same protective effects were also obtained with SCs transplantation after SCI in vivo.