Search Results (3)

Schwann cells (SCs) play a crucial role in peripheral nerve repair by supporting axonal regeneration and remyelination. While extensive research has been conducted using rodent SCs, increasing attention is being directed toward human SCs due to species-specific differences in phenotypical and functional properties, and accessibility of human SCs derived from diverse sources. A major challenge in translating SC-based therapies for nerve repair lies in the inability to replicate human SC myelination in vitro, posing a significant obstacle to drug discovery and preclinical research. In this study, we compared the myelination capacity of human, rodent, and porcine SCs in various co-culture conditions, including species-matched and cross-species neuronal environments in a serum-free medium. Our results confirmed that rodent and porcine SCs readily myelinate neurites under standard culture conditions after treatment with ascorbic acid for two weeks, whereas human SCs, at least within the four-week observation period, failed to show myelin staining in all co-cultures. Furthermore, we investigated whether cell culture manipulation impairs human SC myelination by transplanting freshly harvested and predegenerated human nerve segments into NOD-SCID mice for four weeks. Despite supporting host axonal regeneration into the grafts, human SCs exhibited very limited myelination, suggesting an intrinsic species-specific restriction rather than a cell culture-induced defect. These observations suggest fundamental differences between human and rodent SCs and highlight the need for human-specific models and protocols to advance our understanding of SC myelination. Full article

Following spinal cord injury (SCI), the regenerative capacity of the central nervous system (CNS) is severely limited by the failure of axonal regeneration. The regeneration of CNS axons has been shown to occur by grafting predegenerated peripheral nerves (PPNs) and to be promoted by the transplantation of neural precursor cells (NPCs). The introduction of a combinatorial treatment of PPNs and NPCs after SCI has to address the additional problem of glial scar formation, which prevents regenerating axons from leaving the implant and making functional connections. Previously, we discovered that the synthetic sulfoglycolipid Tol-51 inhibits astrogliosis. The objective was to evaluate axonal regeneration and locomotor function improvement after SCI in rats treated with a combination of PPN, NPC, and Tol-51. One month after SCI, the scar tissue was removed and replaced with segments of PPN or PPN+Tol-51; PPN+NPC+Tol-51. The transplantation of a PPN segment favors regenerative axonal growth; in combination with Tol-51 and NPC, 30% of the labeled descending corticospinal axons were able to grow through the PPN and penetrate the caudal spinal cord. The animals treated with PPN showed significantly better motor function. Our data demonstrate that PPN implants plus NPC and Tol-51 allow successful axonal regeneration in the CNS. Full article

Introduction: Primate animal models are being utilized to explore novel therapies for spinal cord injuries. This study aimed to evaluate the efficiency of the transplantation of predegenerated nerve segments in unilateral spinal cord-hemisected bonnet monkeys’ (Macaca radiata) locomotor functions using the complex runways. Materials and Methods: The bonnet monkeys were initially trained to walk in a bipedal motion on grid and staircase runways. In one group of trained monkeys, surgical hemisection was made in the spinal cord at the T12-L1 level. In the other group, hemisection was induced in the spinal cord, and the ulnar nerve was also transected at the same time (transplant group). After one week, the hemisected cavity was reopened and implanted with predegenerated ulnar nerve segments obtained from the same animal of the transplant group. Results: All the operated monkeys showed significant deficits in locomotion on runways at the early postoperative period. The walking ability of operated monkeys was found to be gradually improved, and they recovered nearer to preoperative level at the fourth postoperative month, and there were no marked differences. Conclusion: The results demonstrate that there were no significant improvements in the locomotion of monkeys on runways after the delayed grafting of nerve segments until one year later. The failure of the predegenerated nerve graft as a possible therapeutic strategy to improve the locomotion of monkeys may be due to a number of factors set in motion by trauma, which could possibly prevent the qualities of regeneration. The exact reason for this ineffectiveness of predegenerated nerve segments and their underlying mechanism is not known. Full article