Tenascin C and Tenascin R, are two proteins that have been the topic of investigation at Ruhr-Universität Bochum. Myelin sheaths, or the sheaths of the nerve cells, are destroyed by immune system cells in this condition.
The renewal of the myelin sheaths is prevented if there are two tenascins, as the Bochum team demonstrated in studies using mice.
The journal “Cells,” which was released online on May 28th, 2022, contains a report on the research by Dr Juliane Bauch and Professor Andreas Faissner of the Cell Morphology and Molecular Neurobiology Department in Bochum.
There is currently no known cause for why multiple sclerosis causes the myelin sheaths to be destroyed.
“But the organism has various mechanisms at its disposal to partially compensate for the lesions,” says Juliane Bauch who conducted a thorough analysis of this issue for her doctoral thesis. Her study purposes at categorizing approaches that could expand the regeneration of myelin sheaths.
Tenascins impede regeneration of nerve cell envelopes
The extracellular matrix, or the framework in which cells are attached, is made up of tenascin C and tenascin R. The cells that make up the myelin sheaths, like oligodendrocytes, are affected by the extracellular matrix.
The researchers gave mice the medication Cuprizone, which eliminates myelin sheaths, to evaluate the impact of the two tenascins on the regeneration of myelin sheaths. Bauch and Faissner kept track of how effectively the myelin sheaths recovered when Cuprizone was stopped.
The procedure was compared in mice that generated tenascin C and tenascin R normally and in mice that were genetically altered to not produce the two tenascins. They cut tissue samples from the brain and measured the myelin sheath thickness for this reason. Mice lacking tenascin C and R were better and faster in regenerating myelin sheaths.
Different effects of the two proteins
Juliane Bauch and Andreas Faissner also looked into how the proteins slowed down the regeneration process. The production of myelin sheaths was constrained by tenascin C. The protein CD68, which promotes acute inflammation, was made more common by tenascin R.
It is also known that both proteins inhibit oligodendrocyte migration. Additionally, they prevent the growth of the protein MBP, which is crucial for the creation of the myelin membrane, during myelin membrane repair.
Our research results open up new therapeutic approaches for the treatment of demyelinating diseases such as multiple sclerosis. The impact of the extracellular matrix on the restoration of myelin membranes is enormous and could become a key target for therapy in the future.”
Dr Juliane Bauch, Cell Morphology and Molecular Neurobiology, Ruhr-Universität Bochum
Bauch, J. & Faissner, A. (2022) The Extracellular Matrix Proteins Tenascin-C and Tenascin-R Retard Oligodendrocyte Precursor Maturation and Myelin Regeneration in a Cuprizone-Induced Long-Term Demyelination Animal Model. Cells. doi.org/10.3390/cells11111773.