Schwann cells will repair axons

Perhaps the nerve processes can be restored

Ilya Khel, Hi-News, based on the materials of the University of Wisconsin–Madison: Study finds a key to nerve regeneration

Scientists from the University of Wisconsin-Madison have discovered a switch that redirects auxiliary cells in the peripheral nervous system into "repair" mode and helps repair damaged axons. Axons are long fibers of neurons that transmit nerve impulses. The peripheral nervous system, a signaling network outside the brain and spinal cord, has some ability to repair damaged axons, but this repair is slow and often to no avail.

A new study suggests tactics that could trigger or accelerate this natural recovery mechanism and help, for example, in treatment after physical injuries, says John Swaren, professor of comparative biosciences at the University of Wisconsin-Madison School of Veterinary Medicine. These results may also be useful for the treatment of genetic abnormalities such as Charcot-Marie-Toute disease or nerve damage from diabetes.

Schwann cells (lemmocytes) create an insulating myelin sheath that accelerates the transmission of nerve impulses. In recovery mode, lemmocytes create a "repair crew" that adds nerve regrowth stimulation to the normal isolation work. Svaren, senior author of a paper published on August 30 in the Journal of Neuroscience (Epigenomic Regulation of Schwann Cell Reprogramming in Peripheral Nerve Injury – VM), studied how lemmocytes hugging axons in the peripheral nervous system are transformed and begin to play a more active and "smart" role after injury.

Svaren and his PhD student Joseph Ma compared the activation of genes in Schwann cells in mice with intact or excised axons. "We saw a set of hidden genes that become active, but only after injury," says Svaren, "and they start a program that puts lemmocytes into recovery mode, in which they perform several types of work necessary for axon regrowth."

In this repair mode, but not in the usual one, Schwann cells begin to clean up the house, helping to dissolve myelin, which is necessary for proper functioning, but ironically interferes with regeneration after injury. "If you invite the Schwann cages to a party," says Svaren, "they'll start putting away bottles and washing dishes until everyone leaves."

This stripping should take place within a few days after the damage, says Svaren. Schwann cells also emit signals that call blood cells to help in cleaning, outline the path of regrowth for the axon. Finally, they return to the role of an insulator, growing a replacement of the myelin sheath on the regenerated axon.

Unexpectedly, it was found that the transition of lemmocytes to the repair form did not involve a return to a more primitive form, but rather was based on a change in the regulation of its genes.

"Almost all other nervous system responses to trauma, especially in the brain, need stem cells to regrow cells, but there are no stem cells here," says Svaren. "Schwann cells reprogram themselves to run an injury repair program. We saw them as active players with a dual role in protecting and regenerating the axon, and we are investigating what factors determine the beginning and effectiveness of the program."

After the human genome was decoded, epigenetics – the study of gene regulation – moved to the forefront. We realized that genes don't really matter if you don't turn them on, and these genetic switches play a crucial role in why skin cells don't look like nerve cells, and nerve cells don't work like blood cells.

In epigenetics, as in the rest of biology, processes are often regulated by the balance between the signals "stand" and "walk". In the case of the Schwann cell transition, Svaren and Ma identified a system called PRC2, which essentially drowns out the repair program. "This path comes down to an on/off switch that is usually off," says Svaren, "and we want to find out how to turn it on to start the recovery process."

The nature of the top-level gene silencer system suggested drugs that could remove the plug label from the genes of interest; Svaren says he has identified an enzyme that can "take off the brakes" and intentionally activate the repair program if necessary to respond to injury.

Even if drug trials are successful, it will take years of experimentation before this system is tested on humans. In addition, it is not completely clear how well the axon can regenerate. It is unlikely that this one track will lead to a panacea, but they hope that it will become important.

Ultimately, this research could open a new door to the regeneration of at least one key sector of the nervous system.

Portal "Eternal youth" http://vechnayamolodost.ru  19.09.2016