Differential regulation of Kir4.1 and Kir2.1 expression in the ischemic rat retina
Differential regulation of Kir4.1 and Kir2.1 expression in the ischemic rat retina
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DOI：
10.1016/j.neulet.2005.11.016
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发表时间：
2006-03-27
影响因子：
2.5
通讯作者：
Bringmann, A
中科院分区：
文献类型：
--
作者：
Iandiev, I;Tenckhoff, S;Bringmann, A
大鼠视网膜缺血再灌注会导致 Muller 细胞神经胶质增生，这与其 K+ 电导的降低有关。通过使用视网膜切片的定量PCR和免疫组织化学染色，我们研究了短暂缺血再灌注对两个内向整流K+(Kir)通道Kir4.1和Kir2.1的视网膜表达的影响。在对照视网膜中，米勒细胞显着表达 Kir4.1 和 Kir2.1 蛋白。再灌注后7天，Kir4.1蛋白表达强烈下调，而Kir2.1蛋白表达保持不变。缺血后Kir4.1 mRNA的表达减少了55%，而Kir2.1 mRNA的表达没有改变。数据表明，不同 Kir 通道的神经胶质表达在视网膜缺血后受到差异性调节，对 K+ 离子和水稳态产生不利影响。 (c) 2005 Elsevier Ireland Ltd. 保留所有权利。
Ischemia-reperfusion of the rat retina causes gliosis of Muller cells that is associated with a decrease of their K+ conductance. By using quantitative PCR and immunohistochemical staining of retinal slices, we investigated the effect of transient ischemia-reperfusion on retinal expression of two inward-rectifying K+ (Kir) channels, Kir4.1 and Kir2.1. In control retinas, Miller cells prominently expressed both Kir4.1 and Kir2.1 proteins. At 7 days after reperfusion, the expression of Kir4.1 protein was strongly downregulated, while the Kir2.1 protein expression remained unaltered. The expression of Kir4.1 mRNA was reduced by 55% after ischemia while the expression of Kir2.1 mRNA was not altered. The data suggest that the glial expression of distinct Kir channels is differentially regulated after retinal ischemia, with deletarious consequences for K+ ion and water homeostasis. (c) 2005 Elsevier Ireland Ltd. All rights reserved.