Schwann cells induce automatic repair of damaged nerves

After an injury, the nerves are often damaged. These nerves are usually regenerated by innate processes. Researchers from the Gutenberg University of Mainz (JGU) and the Swiss University of Friborg have now discovered that Schwann cells and axons could be at the origin of this regeneration process. The results of the study entitled "Injured axons ask Schwann cells to construct constrictive actin spheres to accelerate axon disintegration" were published in the latest issue of the journal Cell reports.

The study was led by Professor Claire Jacob of the Johannes Gutenberg University of Mainz (JGU), who said in a statement: "A lesion of the peripheral nervous system quickly triggers the activation of a fascinating repair process that allows the injured nerve to regenerate and regain its shape. a function. This repair system does not exist in the central nervous system and injuries often result in permanent injuries such as paraplegia ". Professor Jacob is responsible for cellular neurobiology at JGU. She explained that more such strategies could be developed to effectively treat nerve damage.

The team of researchers explains that each of the axons of the nerves is sheathed with myelin. The formation of damaged myelin is the key to regenerating the axon. This myelin around the axon helps the nerve signals to pbad quickly. Jacob said, "Myelin is extremely important for the functioning of the entire nervous system, but it also hinders the process of repairing an injury." The team added that in the peripheral nervous system, this myelin is produced by Schwann cells. in the central nervous system, it is produced by oligodendrocytes. The team wrote that these two types of cells respond differently to injuries. This can cause a difference in the regeneration and healing of injured nerves, explained the team.

Jacob explained that Schwann cells induce the rapid disintegration of axons damaged by damage to the peripheral nervous system. They break the axonal cells into smaller fragments that could be engulfed either by the Schwann cells themselves or by the macrophages being cleaned. The researchers explain that this removal of debris from the damaged axon is the first step in the repair and regeneration process. Claire Jacob said, "Schwann cells can do anything. We discovered that they not only digest myelin after an injury, but that they also induce the disintegration of long axon segments that are separated from their cell body due to injury. "

The team writes that Schwann cells break down broken and segmented axons by making small spheres of proteins known as actin spheres. The team wrote that these spheres exert pressure on the isolated segments of the axon and break them down into smaller pieces. The real need for this process is to remove the damaged part so that the remaining healthy stump of the axon can regrow and join the other side of the broken axon to complete the neural circuit and restore nerve function.

What was new in this study was the discovery that when the axons were broken, they sent signals to Schwann cells to start making the actin spheres and initiate the process of degeneration of the damaged axon regions. The researchers were impressed by the well-coordinated function of the two types of cells repairing the nervous system. They wrote that if communication between the two cell types was disrupted, there was a slowing down of the axon and nerve repair process.

The team then examined the central nervous system and the functioning of oligodendrocytes of regenerating cells. Jacob said, "After an injury, the oligodendrocytes die or remain apparently insensitive." This means that unlike Schwann cells, oligodendrocytes do not trigger to disrupt damaged axons of the central nervous system. The team studied and found that oligodendrocytes do not express VEGFR1 like Schwann cells. Its receptor was responsible for triggering the production of actin spheres in Schwann cells, they noted.

To go further in the experiment, the team has now genetically modified the oligodendrocytes so that these cells can express VEGFR1. They have now noted that oligodendrocytes can now produce actin structures and disrupt broken axon fragments, just like Schwann cells. The team concludes, "These results therefore identify controllable molecular signals of neuron-glia crosstalk essential to the rapid clean up of damaged axons."

Currently, they are working on the molecular level processes that could be responsible for eliminating myelin at injury sites in the hope of reversing it. Jacob said, "We have discovered a pathway that accelerates the degradation of myelin in the peripheral nervous system and we are now trying to determine if this can also trigger the elimination of myelin in the central nervous system."