Grumet M, Friedlander D R, Sakurai T
Department of Pharmacology, New York University Medical Center, New York 10016, USA.
Perspect Dev Neurobiol. 1996;3(4):319-30.
Chondroitin sulfate proteoglycans (CSPGs), including neurocan and phosphocan, are believed to be major components of brain extracellular matrix that interact with other matrix proteins and cell surface receptors. In addition, several brain CSPGs such as receptor protein tyrosine phosphatase beta are expressed as cell surface receptors that interact with proteins in the extracellular matrix and with receptors on neural cells. Recent in vitro studies demonstrate that, although the brain CSPGs neurocan and phosphocan can promote transient adhesion of neuronal cells, they inhibit stable cell adhesion and neurite growth promoted by the cell adhesion molecule Ng-CAM/L1. Neurocan and phosphocan bind with high affinity to Ng-CAM/L1 and N-CAM which may be their major receptors on neurons. These CSPGs also bind to other adhesion molecules, such as tenascin-C, and can differentially modulate adhesion of glia of tenascin-C. Both the glycosaminoglycan and the core glycoproteins contribute to the function of the brain CSPGs. When expressed in regions containing low levels of adhesion molecules, various CSPGs including phosphocan, neurocan, versican, aggrecan, and NG2 proteoglycan may act as barriers to cell migration and axonal growth. In regions containing high levels of adhesion proteins, brain CSPGs may still act to maintain certain boundaries while allowing selective axonal extension to proceed. There are numerous regions of overlap in the expression patterns of CSPGs and adhesion molecules in vivo, and the relative levels of these molecules as well as the organization of the extracellular matrix may be important factors that regulate the rate of axonal growth locally. Differential expression of CSPGs may be important for modulating cell adhesion as well as axonal growth and guidance during neural development, and continued expression may prevent these processes in the normal nature nervous system as well as following brain injury.
硫酸软骨素蛋白聚糖（CSPGs），包括神经黏蛋白和磷酸黏蛋白，被认为是脑细胞外基质的主要成分，可与其他基质蛋白和细胞表面受体相互作用。此外，几种脑CSPGs，如受体蛋白酪氨酸磷酸酶β，作为细胞表面受体表达，可与细胞外基质中的蛋白以及神经细胞上的受体相互作用。最近的体外研究表明，尽管脑CSPGs神经黏蛋白和磷酸黏蛋白可促进神经元细胞的短暂黏附，但它们会抑制细胞黏附分子Ng-CAM/L1促进的稳定细胞黏附和神经突生长。神经黏蛋白和磷酸黏蛋白与Ng-CAM/L1和N-CAM具有高亲和力结合，这可能是它们在神经元上的主要受体。这些CSPGs还与其他黏附分子，如肌腱蛋白-C结合，并可不同程度地调节肌腱蛋白-C对神经胶质细胞黏附的作用。糖胺聚糖和核心糖蛋白都对脑CSPGs的功能有贡献。当在黏附分子水平较低的区域表达时，包括磷酸黏蛋白、神经黏蛋白、多功能蛋白聚糖、聚集蛋白聚糖和NG2蛋白聚糖在内的各种CSPGs可能会成为细胞迁移和轴突生长的障碍。在黏附蛋白水平较高的区域，脑CSPGs可能仍会起到维持某些边界的作用，同时允许选择性轴突延伸继续进行。在体内，CSPGs和黏附分子的表达模式存在许多重叠区域，这些分子的相对水平以及细胞外基质的组织可能是局部调节轴突生长速率的重要因素。CSPGs的差异表达对于调节神经发育过程中的细胞黏附以及轴突生长和导向可能很重要，并且持续表达可能会在正常神经系统以及脑损伤后阻止这些过程。
