A collaborative study led by the Marine Biological Laboratory (MA, USA) has identified molecular pathways involved in spinal cord repair that are common to both lampreys and mammals. The discovery provides new hope for future methods to improve spinal cord injury treatments.
Lampreys are evolutionarily ancient fish that have long been studied for their ability to regenerate neurones, most notably, being able to go from paralysis to full swimming behaviors within 10–12 weeks. “Scientists have known for many years that the lamprey achieves spontaneous recovery from spinal cord injury, but we have not known the molecular recipe that accompanies and supports this remarkable capacity”, explained project collaborator Ona Bloom (Feinstein Institute for Medical Research and the Zucker School of Medicine, NY, USA).
During the study, lampreys were subjected to spinal cord transections and their healing process then monitored, with brain and spinal cord samples being taken from 1 hour post-trauma to 3 months after the event. Researchers discovered that genes expressed in the spinal cord change with recovery, and also observed injury-induced gene expression changes in the brain. These results highlight the long-lasting impact of spinal cord injury on gene expression in the brain, and this data can now potentially be utilized to explore which genes and pathways are essential to the recovery process.
Another major discovery from the study was the observation that many of the genes linked to spinal cord repair are members of the Wnt signaling pathway. To explore this further, the team treated the animals with Wnt-C59, a Wnt inhibitor, discovering that these lampreys were unable to recover their ability to swim. Further studies are planned to explore the particular significance of the Wnt pathway in the healing process.
Sources: Herman PE, Papatheodorou A, Bryant SA, et al. Highly conserved molecular pathways including Wnt signalling, promote functional recovery from spinal cord injury in lampreys. Sci. Rep. doi:10.1038/s41598-017-18757-1. (2018)