Brunden K R, Gregory R, Yoshino J E, Yao J K
Discovery Research Group, Gliatech Inc., Cleveland, Ohio 44122.
Neurochem Res. 1994 Oct;19(10):1277-81. doi: 10.1007/BF01006818.
Schwann cells that are deprived of axonal contact switch their glycolipid metabolic pathway from primarily galactocerebroside (GalCe) synthesis to the formation of glucocerebroside (GlcCe) and its homologs. The removal of axonal influence has a dual effect on Schwann cell phenotype; they lose the ability to assemble both myelin and basement membrane. To determine whether a loss of basement membrane directly affects glycolipid expression, we have examined lipid biosynthesis in Schwann cells which were allowed to interact with axons of dorsal root ganglion neurons but which were deprived of the ability to assemble basal lamina. These Schwann cells resemble those from myelinating nerve in that they synthesize a large amount of galactohydroxycerebroside. This suggests that axon contact, even in the absence of basement membrane, is sufficient to induce the GalCe metabolic pathway.
失去轴突接触的施万细胞会将其糖脂代谢途径从主要合成半乳糖脑苷脂(GalCe)转变为合成葡萄糖脑苷脂(GlcCe)及其同系物。轴突影响的去除对施万细胞表型有双重作用;它们失去了组装髓鞘和基底膜的能力。为了确定基底膜的缺失是否直接影响糖脂表达,我们检测了施万细胞中的脂质生物合成,这些施万细胞被允许与背根神经节神经元的轴突相互作用,但失去了组装基底层的能力。这些施万细胞与有髓神经中的施万细胞相似,因为它们合成大量的半乳糖羟基脑苷脂。这表明,即使在没有基底膜的情况下,轴突接触也足以诱导GalCe代谢途径。