Kobayashi Hideyuki, Yokoo Hiroki, Yanagita Toshihiko, Satoh Shinya, Kis Bela, Deli Maria, Niwa Masami, Wada Akihiko
Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan.
Brain Res. 2006 Dec 6;1123(1):12-9. doi: 10.1016/j.brainres.2006.09.066. Epub 2006 Oct 30.
Water homeostasis in the brain is essential for brain function. We have studied how aquaporin (AQP) 1 expression in GP8 immortalized rat brain microvascular endothelial cells is regulated by glucocorticoid. AQP1 protein level was raised by dexamethasone treatment in a time- and concentration-dependent manner. The up-regulation of AQP1 protein by dexamethasone was associated with an increase of AQP1 mRNA level, with no change in the degradation rate of AQP1 mRNA. AQP1 was concentrated in detergent-insoluble fractions in the cells treated with or without dexamethasone, suggesting that function/trafficking of AQP1 may be regulated via the interaction with lipid rafts. Since glucocorticoid therapy has well known beneficial effects in the treatment of brain edema, the induction of AQP1 by dexamethasone raises a possibility that AQP1 plays a role in ameliorating brain edema.
大脑中的水平衡对于脑功能至关重要。我们研究了糖皮质激素如何调节GP8永生化大鼠脑微血管内皮细胞中aquaporin（AQP）1的表达。地塞米松处理以时间和浓度依赖性方式提高了AQP1蛋白水平。地塞米松对AQP1蛋白的上调与AQP1 mRNA水平的增加相关，而AQP1 mRNA的降解速率没有变化。在用地塞米松处理或未处理的细胞中，AQP1都集中在去污剂不溶性组分中，这表明AQP1的功能/运输可能通过与脂筏的相互作用来调节。由于糖皮质激素疗法在治疗脑水肿方面具有众所周知的有益作用，地塞米松对AQP1的诱导增加了AQP1在减轻脑水肿中起作用的可能性。
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