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Article

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

Department of Cell Morphology and Molecular Neurobiology, Ruhr-University Bochum, Universitätsstr. 150, 44801 Bochum, Germany
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Author to whom correspondence should be addressed.
Academic Editor: Markus Kipp
Cells 2022, 11(11), 1773; https://doi.org/10.3390/cells11111773
Received: 1 April 2022 / Revised: 16 May 2022 / Accepted: 20 May 2022 / Published: 28 May 2022
(This article belongs to the Collection Oligodendrocyte Physiology and Pathology Function)
Oligodendrocytes are the myelinating cells of the central nervous system. The physiological importance of oligodendrocytes is highlighted by diseases such as multiple sclerosis, in which the myelin sheaths are degraded and the axonal signal transmission is compromised. In a healthy brain, spontaneous remyelination is rare, and newly formed myelin sheaths are thinner and shorter than the former ones. The myelination process requires the migration, proliferation, and differentiation of oligodendrocyte precursor cells (OPCs) and is influenced by proteins of the extracellular matrix (ECM), which consists of a network of glycoproteins and proteoglycans. In particular, the glycoprotein tenascin-C (Tnc) has an inhibitory effect on the differentiation of OPCs and the remyelination efficiency of oligodendrocytes. The structurally similar tenascin-R (Tnr) exerts an inhibitory influence on the formation of myelin membranes in vitro. When Tnc knockout oligodendrocytes were applied to an in vitro myelination assay using artificial fibers, a higher number of sheaths per single cell were obtained compared to the wild-type control. This effect was enhanced by adding brain-derived neurotrophic factor (BDNF) to the culture system. Tnr−/− oligodendrocytes behaved differently in that the number of formed sheaths per single cell was decreased, indicating that Tnr supports the differentiation of OPCs. In order to study the functions of tenascin proteins in vivo Tnc−/− and Tnr−/− mice were exposed to Cuprizone-induced demyelination for a period of 10 weeks. Both Tnc−/− and Tnr−/− mouse knockout lines displayed a significant increase in the regenerating myelin sheath thickness after Cuprizone treatment. Furthermore, in the absence of either tenascin, the number of OPCs was increased. These results suggest that the fine-tuning of myelin regeneration is regulated by the major tenascin proteins of the CNS. View Full-Text
Keywords: tenascin-C; tenascin-R; myelin; oligodendrocyte; myelin lesion; cuprizone tenascin-C; tenascin-R; myelin; oligodendrocyte; myelin lesion; cuprizone
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MDPI and ACS Style

Bauch, J.; Faissner, A. 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 2022, 11, 1773. https://doi.org/10.3390/cells11111773

AMA Style

Bauch J, Faissner A. 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. 2022; 11(11):1773. https://doi.org/10.3390/cells11111773

Chicago/Turabian Style

Bauch, Juliane, and Andreas Faissner. 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 11, no. 11: 1773. https://doi.org/10.3390/cells11111773

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