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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 >Functional expression of choline transporter-like protein 1 (CTL1) in human neuroblastoma cells and its link to acetylcholine synthesis.
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Functional expression of choline transporter-like protein 1 (CTL1) in human neuroblastoma cells and its link to acetylcholine synthesis.

机译：胆碱转运蛋白样蛋白1（CTL1）在人类神经母细胞瘤细胞中的功能性表达及其与乙酰胆碱合成的联系。

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摘要

We examined the molecular and functional characterization of choline uptake into human neuroblastoma cell lines (SH-SY5Y: non-cholinergic and LA-N-2: cholinergic neuroblastoma), and the association between choline transport and acetylcholine (ACh) synthesis in these cells. Choline uptake was saturable and mediated by a single transport system. Removal of Na(+) from the uptake buffer strongly enhanced choline uptake. Choline uptake was inhibited by the choline analogue hemicholinium-3 (HC-3) and various organic cations, and was significantly decreased by acidification of the extracellular medium. The increase in choline uptake under Na(+)-free conditions was inhibited by a Na(+)/H(+) exchanger (NHE) inhibitor. Real-time PCR revealed that choline transporter-like protein 1 (CTL1), NHE1 and NHE5 mRNA are mainly expressed. Western blot and immunocytochemical analysis indicated that CTL1 protein was expressed in plasma membrane. ChAT mRNA was expressed at a much higher level in LA-N-2 cells than in SH-SY5Y cells. The conversion of choline to ACh was confirmed in both cells, and was enhanced in Na(+)-free conditions. These findings suggest that CTL1 is functionally expressed in both SH-SY5Y and LA-N-2 cells and is responsible for choline uptake that relies on a directed H(+) gradient as a driving force, and this transport functions in co-operation with NHE1 and NHE5. Furthermore, choline uptake through CTL1 is associated with ACh synthesis in cholinergic neuroblastoma cells.
机译：我们检查了人类神经母细胞瘤细胞系（SH-SY5Y：非胆碱能和LA-N-2：胆碱能神经母细胞瘤）中胆碱摄取的分子和功能特征，以及这些细胞中胆碱转运与乙酰胆碱（ACh）合成之间的关联。胆碱的摄取是饱和的，并由单一转运系统介导。从摄取缓冲液中去除Na（+）可以大大增强胆碱的摄取。胆碱类似物hemicholinium-3（HC-3）和各种有机阳离子可抑制胆碱的摄取，并且通过细胞外培养基的酸化作用可显着降低胆碱的摄取。 Na（+）/ H（+）交换剂（NHE）抑制剂抑制在无Na（+）的条件下胆碱摄取的增加。实时荧光定量PCR显示胆碱转运蛋白样蛋白1（CTL1），NHE1和NHE5 mRNA的主要表达。 Western blot和免疫细胞化学分析表明CTL1蛋白在质膜中表达。 ChAT mRNA在LA-N-2细胞中的表达水平比在SH-SY5Y细胞中高得多。在两个细胞中均证实胆碱向ACh的转化，并在无Na（+）的条件下得到增强。这些发现表明，CTL1在SH-SY5Y和LA-N-2细胞中均功能性表达，并负责胆碱的摄取，胆碱的摄取依赖于定向H（+）梯度作为驱动力，并且这种转运与NHE1和NHE5。此外，胆碱能神经母细胞瘤细胞中通过CTL1摄取胆碱与ACh的合成有关。

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