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C1ql1 expression in oligodendrocyte progenitor cells promotes oligodendrocyte differentiation

少突胶质细胞 多发性硬化 神经科学 髓鞘 生物 祖细胞 表型 祖细胞 细胞分化 细胞生物学 干细胞 免疫学 中枢神经系统 基因 遗传学
作者
Zeynep M. Altunay,Joyshree Biswas,Hiu Wing Cheung,Robert S. Pijewski,Lucille E. Papile,Yetunde O. Akinlaja,Andrew Tang,Lyndsay C. Kresic,Alexander D. Schouw,Maksym V. Ugrak,Keaven Caro,Perla A. Peña Palomino,Susanne Ressl,Akiko Nishiyama,Stephen J. Crocker,David C. Martinelli
出处
期刊:FEBS Journal [Wiley]
被引量:4
标识
DOI:10.1111/febs.17256
摘要

Myelinating oligodendrocytes arise from the stepwise differentiation of oligodendrocyte progenitor cells (OPCs). Approximately 5% of all adult brain cells are OPCs. Why would a mature brain need such a large number of OPCs? New myelination is possibly required for higher‐order functions such as cognition and learning. Additionally, this pool of OPCs represents a source of new oligodendrocytes to replace those lost during injury, inflammation, or in diseases such as multiple sclerosis (MS). How OPCs are instructed to differentiate into oligodendrocytes is poorly understood, and for reasons presently unclear, resident pools of OPCs are progressively less utilized in MS. The complement component 1, q subcomponent‐like (C1QL) protein family has been studied for their functions at neuron–neuron synapses, but we show that OPCs express C1ql1 . We created OPC‐specific conditional knockout mice and show that C1QL1 deficiency reduces the differentiation of OPCs into oligodendrocytes and reduces myelin production during both development and recovery from cuprizone‐induced demyelination. In vivo over‐expression of C1QL1 causes the opposite phenotype: increased oligodendrocyte density and myelination during recovery from demyelination. We further used primary cultured OPCs to show that C1QL1 levels can bidirectionally regulate the extent of OPC differentiation in vitro . Our results suggest that C1QL1 may initiate a previously unrecognized signaling pathway to promote differentiation of OPCs into oligodendrocytes. This study has relevance for possible novel therapies for demyelinating diseases and may illuminate a previously undescribed mechanism to regulate the function of myelination in cognition and learning.
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