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缺血再灌注后诱导型星形胶质细胞葡萄糖转运蛋白-3有助于增强细胞内糖原的储存。

Inducible astrocytic glucose transporter-3 contributes to the enhanced storage of intracellular glycogen during reperfusion after ischemia.

机构信息

Laboratory of Cellular Cybernetics, Graduate School of Information Science and Technology, Hokkaido University, Sapporo 060-0814, Japan.

出版信息

Neurochem Int. 2011 Aug;59(2):319-25. doi: 10.1016/j.neuint.2011.06.006. Epub 2011 Jun 15.

DOI:10.1016/j.neuint.2011.06.006
PMID:21703319
Abstract

Glucose is a necessary source of energy to sustain cell activities and homeostasis in the brain, and enhanced glucose transporter (GLUT) activities are protective of cells during energy depletion including brain ischemia. Here we investigated whether and if so how the astrocytic expression of GLUTs crucial for the uptake of glucose changes in ischemic conditions. Under physiological conditions, cultured astrocytes primarily expressed GLUT1, and GLUT3 was only detected at extremely low levels. However, exposure to ischemic stress increased the expression of not only GLUT1 but also GLUT3. During ischemia, cultured astrocytes significantly increased production of the transcription factor nuclear factor-κB (NF-κB), leading to an increase in GLUT3 expression. Moreover, astrocytic GLUT3 was responsible for the enhanced storage of intracellular glucose during reperfusion, resulting in increased resistance to lethal ischemic stress. These results suggested that astrocytes promptly increase GLUT3 production in situations such as ischemia, and much glucose is quickly taken up, possibly contributing to the protection of astrocytes from ischemic damage.

摘要

葡萄糖是维持大脑细胞活动和内稳态所必需的能量来源,增强葡萄糖转运蛋白(GLUT)的活性可以在能量耗竭包括脑缺血时保护细胞。在这里,我们研究了在缺血条件下,对葡萄糖摄取至关重要的星形胶质细胞 GLUT 的表达是否以及如何发生变化。在生理条件下,培养的星形胶质细胞主要表达 GLUT1,而 GLUT3 仅以极低的水平检测到。然而,暴露于缺血应激不仅增加了 GLUT1 的表达,而且还增加了 GLUT3 的表达。在缺血期间,培养的星形胶质细胞显著增加了转录因子核因子-κB(NF-κB)的产生,导致 GLUT3 表达增加。此外,星形胶质细胞 GLUT3 负责在再灌注期间增强细胞内葡萄糖的储存,从而增加对致命性缺血应激的抵抗力。这些结果表明,星形胶质细胞在缺血等情况下会迅速增加 GLUT3 的产生,大量的葡萄糖被迅速摄取,可能有助于保护星形胶质细胞免受缺血损伤。

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