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NG2 蛋白聚糖促进少突胶质前体细胞增殖和发育性髓鞘形成。

The NG2 proteoglycan promotes oligodendrocyte progenitor proliferation and developmental myelination.

机构信息

Burnham Institute for Medical Research, 10901 N Torrey Pines Road, La Jolla, CA 92037, USA.

出版信息

Neuroscience. 2010 Mar 10;166(1):185-94. doi: 10.1016/j.neuroscience.2009.12.014. Epub 2009 Dec 16.

Abstract

The NG2 proteoglycan has been shown to promote proliferation and motility in a variety of cell types. The presence of NG2 on oligodendrocyte progenitor cells (OPCs) suggests that the proteoglycan may be a factor in expansion of the OPC pool to fill the entire CNS prior to OPC differentiation to form myelinating oligodendrocytes. Comparisons of postnatal cerebellar myelination in wild type and NG2 null mice reveal reduced numbers of OPCs in developing white matter of the NG2 null mouse. Quantification of BrdU incorporation shows that reduced proliferation is a key reason for this OPC shortage, with the peak of OPC proliferation delayed by 4-5 days in the absence of NG2. As a result of the subnormal pool of OPCs, there is also a delay in production of mature oligodendrocytes and myelinating processes in the NG2 null cerebellum. NG2 may promote OPC proliferation via enhancement of growth factor signaling or mediation of OPC interaction with unmyelinated axons.

摘要

NG2 蛋白聚糖已被证明能促进多种细胞类型的增殖和迁移。少突胶质前体细胞(OPC)上存在 NG2,提示该蛋白聚糖可能是 OPC 池扩张的一个因素,以在 OPC 分化形成髓鞘形成少突胶质细胞之前填满整个中枢神经系统。对野生型和 NG2 缺失型小鼠出生后小脑髓鞘形成的比较显示,NG2 缺失型小鼠发育中的白质中 OPC 数量减少。BrdU 掺入的定量分析表明,增殖减少是 OPC 短缺的一个关键原因,在没有 NG2 的情况下,OPC 增殖的高峰期延迟了 4-5 天。由于 OPC 池的数量低于正常水平,NG2 缺失型小脑也会延迟成熟少突胶质细胞和髓鞘形成过程的产生。NG2 可能通过增强生长因子信号或调节 OPC 与未髓鞘化轴突的相互作用来促进 OPC 增殖。

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