Glanville N T, Byers D M, Cook H W, Spence M W, Palmer F B
Atlantic Research Centre for Mental Retardation, Halifax, Canada.
Biochim Biophys Acta. 1989 Aug 8;1004(2):169-79. doi: 10.1016/0005-2760(89)90265-8.
Phosphoinositide and inositol metabolism was compared in glioma (C6), neuroblastoma (N1E-115) and neuroblastoma X glioma hybrid (NG 108-15) cells. All cell lines had similar proportions of phosphatidylinositol (PI), phosphatidylinositol 4-phosphate (PIP), and phosphatidylinositol 4,5-bisphosphate (PIP2). Neuroblastoma and hybrid cells had almost identical phospholipid and phosphoinositide compositions and similar activities for the enzymes metabolizing polyphosphoinositides (PI kinase, PIP phosphatase, PIP kinase, PIP2 phosphatase, PIP2 phosphodiesterase). Glioma cells differed by having greater proportions of ethanolamine plasmalogen and sphingomyelin, lower PIP kinase, 3-5-fold higher PIP phosphatase activity and 10-15-fold greater PIP2 phosphodiesterase activity. Higher PIP phosphatase and PIP2 diesterase activities appear to be characteristic of cells of glial origin, since similar activities were found in primary cultures of astroglia. Glioma cells also metabolize inositol differently. In pulse and pulse-chase experiments, glioma cells transported inositol into a much larger water-soluble intracellular pool and maintained a concentration gradient 30-times greater than neuroblastoma cells. Label in intracellular inositol was less than in phosphoinositides in neuroblastoma and exchanged rapidly with extracellular inositol. In glioma, labeling of intracellular inositol greatly exceeded that of phosphoinositides. As a consequence, radioactivity in prelabeled phosphoinositides could not be effectively chased from glioma cells by excess unlabeled inositol. Such differences between cells of neuronal and glial origin suggest different and possibly supportive roles for these two cell types in maintaining functions regulated through phosphoinositide-linked signalling systems in the central nervous system.
对胶质瘤（C6）、神经母细胞瘤（N1E - 115）和神经母细胞瘤X胶质瘤杂交瘤（NG 108 - 15）细胞中的磷酸肌醇和肌醇代谢进行了比较。所有细胞系中磷脂酰肌醇（PI）、磷脂酰肌醇4 - 磷酸（PIP）和磷脂酰肌醇4,5 - 二磷酸（PIP2）的比例相似。神经母细胞瘤和杂交瘤细胞具有几乎相同的磷脂和磷酸肌醇组成，以及代谢多磷酸肌醇的酶（PI激酶、PIP磷酸酶、PIP激酶、PIP2磷酸酶、PIP2磷酸二酯酶）的相似活性。胶质瘤细胞的不同之处在于乙醇胺缩醛磷脂和鞘磷脂的比例更高，PIP激酶较低，PIP磷酸酶活性高3 - 5倍，PIP2磷酸二酯酶活性高10 - 15倍。较高的PIP磷酸酶和PIP2二酯酶活性似乎是神经胶质起源细胞的特征，因为在星形胶质细胞的原代培养物中也发现了类似的活性。胶质瘤细胞对肌醇的代谢也不同。在脉冲和脉冲追踪实验中，胶质瘤细胞将肌醇转运到一个大得多的水溶性细胞内池中，并维持比神经母细胞瘤细胞大30倍的浓度梯度。神经母细胞瘤细胞内肌醇的标记量少于磷酸肌醇中的标记量，并且能与细胞外肌醇快速交换。在胶质瘤中，细胞内肌醇的标记量大大超过磷酸肌醇中的标记量。因此，过量的未标记肌醇无法有效地从胶质瘤细胞中追踪预先标记的磷酸肌醇中的放射性。神经源性和胶质源性细胞之间的这种差异表明这两种细胞类型在维持通过中枢神经系统中磷酸肌醇连接信号系统调节的功能方面具有不同且可能相互支持的作用。
