NG2 colocalizes with axons and is expressed by a mixed cell population in spinal cord lesions
NG2 colocalizes with axons and is expressed by a mixed cell population in spinal cord lesions
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DOI：
10.1097/01.jnen.0000218447.32320.52
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发表时间：
2006-04-01
影响因子：
3.2
通讯作者：
Wei, Ping
中科院分区：
文献类型：
--
作者：
McTigue, Dana M.;Tripathi, Richa;Wei, Ping
NG 2蛋白聚糖在脊髓损伤后受到普遍关注，因为它由有助于中枢神经系统髓鞘再生的少突胶质细胞祖细胞（OPC）表达;然而，NG 2可能抑制轴突再生。我们和其他人研究了脊髓损伤（SCI）后NG 2的时空表达。在这里，我们扩展了这些观察，并提供了一个全面的分析的分布，表型，和共同定位的NG 2细胞与轴突在临床相关模型的脊髓挫伤。由于挫伤模型模拟了大多数人类SCI，因此这些信息对于理解促进和/或阻止修复的内源性过程非常重要。数据表明，NG 2水平显着上升3和7天之间的伤后（dpi），并保持在整个病变慢性升高。病变内的NG 2可以来源于一系列浸润细胞;因此，使用一组抗体来研究NG 2细胞表型。首先，检查血小板衍生生长因子-α受体（PDGF α R）共定位，因为OPCs通常表达两种标记物。PDGFaR细胞在检查的所有时间均存在于病变中。然而，在14 dpi时，只有37%的NG 2细胞共表达PDGF α R，到70 dpi时降至< 1%。这与病变周围的备用组织几乎完全重叠形成对比。相反，40%至60%的NG 2细胞表达p75，约84%表达Sox 10，表明许多NG 2细胞是非髓鞘形成的雪旺细胞。尽管NG 2水平不断升高，我们注意到轴突在病变中有强劲而持续的生长，其中许多轴突位于沿着NG 2轮廓。因此，脊髓挫伤产生了一个富含NG 2的环境，轴突在其中生长，并且其中NG 2的来源与周围备用组织中的NG 2来源明显不同。
The NG2 proteoglycan is of general interest after spinal cord injury because it is expressed by oligodendrocyte progenitors (OPCs), which contribute to central nervous system remyelination; however, NG2 may inhibit axon regeneration. We and others have examined the spatiotemporal expression of NG2 after spinal cord injury (SCI). Here, we extend those observations and provide a comprehensive analysis of the distribution, phenotype, and colocalization of NG2 cells with axons in a clinically relevant model of spinal contusion. Because contusion models mimic the majority of human SCI, this information is important for understanding endogenous processes that promote and/or prevent repair. The data demonstrate that NG2 levels rise significantly between 3 and 7 days postinjury (dpi) and remain elevated chronically throughout the lesions. NG2 within the lesions could be derived from an array of infiltrating cells; thus, a panel of antibodies was used to investigate NG2 cell phenotypes. First, platelet-derived growth factor-alpha receptor (PDGF alpha R) colocalization was examined because OPCs normally express both markers. PDGFaR cells were present in lesions at all times examined. However, only 37% of NG2 cells coexpressed PDGF alpha R at 14 dpi, which dropped to < 1% by 70 dpi. This contrasts with the nearly complete overlap in spared tissue surrounding the lesion. In contrast, 40% to 60% of NG2 cells expressed p75 and approximately 84% expressed Sox 10, suggesting that many NG2 cells were nonmyelinating Schwann cells. Despite rising levels of NG2, we noted robust and sustained axon growth into the lesions, many of which were located along NG2 profiles. Thus, spinal contusion produces an NG2-rich environment into which axons grow and in which the source of NG2 appears considerably different from that in surrounding spared tissue.