Evidence That DDR1 Promotes Oligodendrocyte Differentiation during Development and Myelin Repair after Injury

Oligodendrocytes generate myelin sheaths vital for the formation, health, and function of the central nervous system. Mounting evidence suggests that receptor tyrosine kinases (RTKs) are crucial for oligodendrocyte differentiation and myelination in the CNS. It was recently reported that discoidin d...

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Bibliographic Details
Published in:International journal of molecular sciences 2023-06, Vol.24 (12), p.10318
Main Authors: Mei, Ruyi, Qiu, Wanwan, Yang, Yingying, Xu, Siyu, Rao, Yueyu, Li, Qingxin, Luo, Yuhao, Huang, Hao, Yang, Aifen, Tao, Huaping, Qiu, Mengsheng, Zhao, Xiaofeng
Format: Article
Language:English
Subjects:
Ablation
AKT protein
Alzheimer's disease
Animals
Cell Differentiation
Central Nervous System
Ddr1
Demyelinating diseases
Demyelination
Differentiation
Discoidin Domain Receptor 1 - genetics
Discoidin Domain Receptor 1 - metabolism
ERK
Female
Kinases
Male
Mice
Mice, Knockout
Motor ability
Mutation
Myelin
Myelin Sheath - metabolism
Myelination
Nervous system
Neurogenesis
oligodendrocyte
Oligodendrocytes
Oligodendroglia - metabolism
Receptor Protein-Tyrosine Kinases - metabolism
Sheaths
Tyrosine
Young adults
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Summary:Oligodendrocytes generate myelin sheaths vital for the formation, health, and function of the central nervous system. Mounting evidence suggests that receptor tyrosine kinases (RTKs) are crucial for oligodendrocyte differentiation and myelination in the CNS. It was recently reported that discoidin domain receptor 1 (Ddr1), a collagen-activated RTK, is expressed in oligodendrocyte lineage. However, its specific expression stage and functional role in oligodendrocyte development in the CNS remain to be determined. In this study, we report that is selectively upregulated in newly differentiated oligodendrocytes in the early postnatal CNS and regulates oligodendrocyte differentiation and myelination. knock-out mice of both sexes displayed compromised axonal myelination and apparent motor dysfunction. deficiency alerted the ERK pathway, but not the AKT pathway in the CNS. In addition, function is important for myelin repair after lysolecithin-induced demyelination. Taken together, the current study described, for the first time, the role of in myelin development and repair in the CNS, providing a novel molecule target for the treatment of demyelinating diseases.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms241210318