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首页> 外文期刊>Journal of Cellular Physiology >BDNF regulates GLAST and glutamine synthetase in mouse retinal Muller cells.
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BDNF regulates GLAST and glutamine synthetase in mouse retinal Muller cells.

机译：脑源性神经营养因子调节GLAST和谷氨酰胺合成酶老鼠视网膜Muller细胞。

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摘要

This study investigated whether brain-derived neurotrophic factor (BDNF) regulates the L-glutamate/L-aspartate transporter (GLAST) and glutamine synthetase (GS) in mouse retinal Muller cells (RMCs) under normal and hypoxic conditions. Mouse RMCs were treated with recombinant human BDNF (50, 75, 100, 125, or 150 ng/ml) for 24 h or underwent hypoxia induced by CoCl(2) (125 microM; 6, 12, 24, 48, or 72 h). An additional group underwent combined treatment with BDNF (100 ng/ml; 24, 48, 72, or 96 h) and CoCl(2) (125 microM/ml; 72 h). GLAST and GS mRNA and protein expression, L-[3,4-3H]-glutamic acid uptake, and apoptosis were assessed. BDNF dose-dependently up-regulated GLAST and GS mRNA and protein and increased glutamate uptake. Similarly, in early-stage CoCl(2)-induced hypoxia, GLAST and GS were up-regulated and glutamate uptake increased, but these decreased over time. BDNF also up-regulated GLAST and GS and increased glutamate uptake when RMCs under CoCl(2) induced hypoxic condition. However, BDNF treatment 24 h before CoCl(2) had no effect on GLAST or GS expression. CoCl(2) alone or combined with BDNF did not induce apoptosis. Hypoxia rapidly increased GLAST and GS expressions. This effect was transient, perhaps due to compensatory mechanisms that reduce GLAST and GS by 72 h. BDNF can up-regulate GLAST and GS and increase glutamate uptake during hypoxia, and these functions may underlie its neuroprotective effects.
机译：本研究调查是否脑源性神经营养因子(BDNF)调节的L-glutamate / L-aspartate运输车(GLAST)和谷氨酰胺合成酶(GS)在小鼠视网膜穆勒细胞在正常和缺氧条件下(rmc)。鼠标rmc重组体人对待脑源性神经营养因子(50、75、100、125或150 ng / ml) 24 h或经历了缺氧引起CoCl (2) (125 microM;6、12、24、48或72 h)。另一个组经历了与BDNF联合治疗(100ng / ml;microM /毫升;表情,L - 3 4-3H谷氨酸酸吸收,和细胞凋亡被评估。差异GLAST GS mRNA和蛋白谷氨酸摄取增加。早期CoCl(2)全身缺氧,GLAST和GS差异和谷氨酸摄取增加,但这些随着时间的减少。差异GLAST GS和增加谷氨酸rmc在吸收CoCl(2)诱导缺氧条件。GLAST CoCl(2)没有影响或GS表达式。CoCl(2)单独或结合BDNF没有诱导细胞凋亡。和GS表达式。或许是由于补偿机制减少72 h。GLAST和GS BDNF可以调控的GLAST和GS和谷氨酸摄取增加缺氧,这些功能可能是它的基础神经保护作用。

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