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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >The regulation of glycine transporter GLYT1 is mainly mediated by protein kinase Calpha in C6 glioma cells.
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The regulation of glycine transporter GLYT1 is mainly mediated by protein kinase Calpha in C6 glioma cells.

机译：甘氨酸转运蛋白GLYT1的调节主要由C6胶质瘤细胞中的蛋白激酶Calpha介导。

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摘要

Glycine has been shown to possess important functions as a bidirectional neurotransmitter. At synaptic clefts, the concentration of glycine is tightly regulated by the uptake of glycine released from nerve terminals into glial cells by the transporter GLYT1. It has been recently demonstrated that protein kinase C (PKC) mediates the downregulation of GLYT1 activity in several cell systems. However, it remains to be elucidated which subtypes of PKC might be important in the regulation of GLYT1 activity. In this study, we attempted to make clear the mechanism of the phorbol 12-myristate 13-acetate (PMA)-suppressed uptake of glycine in C6 glioma cells which have the native expression of GLYT1. In C6 cells, the expression of PKCalpha, PKCdelta, and PKCvarepsilon of the PMA-activated subtypes was detected. The PMA-suppressed action was fully reversed by the removal of both extracellular and intracellular Ca(2+). Furthermore, the inhibitory effects of PMA or thymeleatoxin (THX), which is a selective activatorof conventional PKC (cPKC), were blocked by the downregulation of all PKCs expressed in C6 cells by long-term incubation with THX, or pretreatment with GF109203X or Go6983, which are broad inhibitors of PKC, or Go6976, a selective inhibitor of cPKC. On the other hand, treatment of C6 cells with ingenol, a selective activator of novel PKCs, especially PKCdelta and PKCvarepsilon, did not affect the transport of glycine. Silencing of PKCdelta expression by using RNA interference or pretreatment with the inhibitor peptide for PKCvarepsilon had no effect on the PMA-suppressed uptake of glycine. Together, these results suggest PKCalpha to be a crucial factor in the regulation of glycine transport in C6 cells.
机译：甘氨酸已显示出作为双向神经递质的重要功能。在突触裂隙中，甘氨酸的浓度受到转运蛋白GLYT1从神经末梢释放到神经胶质细胞中的甘氨酸的摄取的严格控制。最近已经证明，蛋白激酶C（PKC）介导了几种细胞系统中GLYT1活性的下调。但是，仍有待阐明哪些PKC亚型可能在GLYT1活性的调节中很重要。在这项研究中，我们试图弄清楚佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）抑制具有天然表达GLYT1的C6胶质瘤细胞摄取甘氨酸的机制。在C6细胞中，检测到PMA激活亚型的PKCalpha，PKCdelta和PKCvarepsilon的表达。通过移除细胞外和细胞内Ca（2+），完全逆转了PMA抑制的作用。此外，PMA或作为常规PKC（cPKC）选择性激活剂的胸腺四恶精（THX）的抑制作用通过与THX长期孵育或用GF109203X或Go6983预处理而被C6细胞中表达的所有PKC下调而被阻断，它们是PKC的广泛抑制剂或Go6976（cPKC的选择性抑制剂）。另一方面，用新的PKCs，特别是PKCdelta和PKCvarepsilon的选择性激活剂-丁二酚对C6细胞进行处理不会影响甘氨酸的转运。通过使用RNA干扰或用PKCvarepsilon抑制剂肽预处理来沉默PKCdelta表达，对PMA抑制的甘氨酸摄取没有影响。总之，这些结果表明PKCalpha是调节C6细胞中甘氨酸转运的关键因素。

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