. Scientific Frontline: Tenascin proteins inhibit cell sheath regeneration

Friday, June 17, 2022

Tenascin proteins inhibit cell sheath regeneration

Juliane Bauch (left) and Andreas Faissner from the Chair of Cell Morphology and Molecular Neurobiology
Credit: RUB, Kramer

In multiple sclerosis, nerve cells lose their insulating layer. Researchers from Bochum are looking for starting points to promote regeneration processes. They have identified two relevant proteins.

Researchers at the Ruhr University Bochum have investigated the role that the two proteins tenascin C and tenascin R play in multiple sclerosis. In the disease, cells of the immune system destroy the myelin sheaths, i.e. the sheathing of the nerve cells. As the Bochum team showed in experiments with mice, the presence of the two Tenascins inhibits the regeneration of the myelin sheaths. Dr. Juliane Bauch and Prof. Dr. Andreas Faissner from the Bochum Chair for Cell Morphology and Molecular Neurobiology describes the results in the journal Cells.

The cause of the destruction of myelin sheaths in multiple sclerosis has not yet been clarified. "But the organism has various mechanisms to partially compensate for the lesions," says Juliane Bauch, who dealt intensively with the topic in her doctorate. The aim of the work is to identify starting points with which the regeneration of myelin sheaths could be improved.

Tenascins hinder regeneration of the nerve cell sheathing

Tenascin C and Tenascin R are components of the extracellular matrix, i.e. the framework in which the cells are embedded. The extracellular matrix influences the cells, such as the oligodendrocytes, which form the myelin sheaths. In order to investigate the influence of the two tenascins on the regeneration of the myelin sheaths, the researchers treated mice with the agent cuprizon, which destroys the myelin sheaths. After Cuprizon was discontinued, Bauch and Faissner observed how well the myelin sheaths regenerated.

The researchers compared the process in mice that made tenascin C and tenascin R normal and in genetically modified mice that lacked the two tenascins. For this purpose, they created tissue sections of the brain and evaluated the thickness of the myelin sheaths. Mice without Tenascin C and R were able to rebuild myelin sheaths faster and more successfully.

Different effects of the two proteins

Juliane Bauch and Andreas Faissner also examined the mechanisms with which the proteins hindered the regeneration process. Tenascin C limited the number of myelin sheaths formed. Tenascin R favored the presence of the CD68 protein, which drives acute inflammation. Both proteins are also known to limit the movements of oligodendrocytes. They also limit the formation of the MBP protein, which is important for the formation of myelin membranes, during the restoration of the myelin membranes.

“Our research results open up new therapeutic approaches for the treatment of demyelinating diseases such as multiple sclerosis. The influence of the extracellular matrix on the restoration of the myelin membranes is enormous and could become an important target for therapy in the future,” summarizes Juliane Bauch.

The German Research Foundation funded the work as part of the project with the funding code FA 159 / 24-1, Grant number 407698736.

Source/Credit: Ruhr University Bochum


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