DIFFERENCES IN THE METABOLISM OF INOSITOL AND PHOSPHOINOSITIDES BY CULTURED-CELLS OF NEURONAL AND GLIAL ORIGIN
DIFFERENCES IN THE METABOLISM OF INOSITOL AND PHOSPHOINOSITIDES BY CULTURED-CELLS OF NEURONAL AND GLIAL ORIGIN
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DOI：
10.1016/0005-2760(89)90265-8
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发表时间：
1989-08-08
期刊：
影响因子：
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通讯作者：
PALMER, FBSC
中科院分区：
文献类型：
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作者：
GLANVILLE, NT;BYERS, DM;PALMER, FBSC
在神经胶质瘤（C6）、神经母细胞瘤（N1 E-115）和神经母细胞瘤（N1 E-115）中比较磷酸肌醇和肌醇代谢。胶质瘤杂交细胞（NG 108-15）。所有细胞系具有相似比例的磷脂酰肌醇（PI）、磷脂酰肌醇4-磷酸（PIP）和磷脂酰肌醇4，5-二磷酸（PIP 2）。神经母细胞瘤和杂交细胞具有几乎相同的磷脂和磷酸肌醇组成，并且代谢聚磷酸肌醇的酶（PI激酶、PIP磷酸酶、PIP激酶、PIP 2磷酸酶、PIP 2磷酸二酯酶）具有相似的活性。神经胶质瘤细胞的不同之处在于具有更大比例的乙醇胺缩醛磷脂和鞘磷脂、更低的PIP激酶、3-5倍更高的PIP磷酸酶活性和10-15倍更高的PIP 2磷酸二酯酶活性。较高的PIP磷酸酶和PIP 2二酯酶活性似乎是神经胶质细胞起源的特征，因为在星形胶质细胞的原代培养物中发现了类似的活性。神经胶质瘤细胞也代谢肌醇不同。在脉冲和脉冲追逐实验中，神经胶质瘤细胞将肌醇转运到更大的水溶性细胞内池中，并保持比神经母细胞瘤细胞高30倍的浓度梯度。神经母细胞瘤中细胞内肌醇的标记少于磷酸肌醇，并与细胞外肌醇迅速交换。在胶质瘤中，细胞内肌醇的标记大大超过磷酸肌醇。因此，放射性预标记的磷酸肌醇不能有效地追逐胶质瘤细胞过量的未标记的肌醇。神经元和神经胶质细胞来源的细胞之间的这种差异表明这两种细胞类型在维持中枢神经系统中通过磷酸肌醇连接的信号系统调节的功能中的不同和可能的支持作用。
Phosphoinositide and inositol metabolism was compared in glioma (C6), neuroblastoma (N1E-115) and neuroblastoma .times. 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.