Iandiev Ianors, Tenckhoff Solveig, Pannicke Thomas, Biedermann Bernd, Hollborn Margrit, Wiedemann Peter, Reichenbach Andreas, Bringmann Andreas
Paul Flechsig Institute of Brain Research, University of Leipzig Medical Faculty, Jahnallee 59, 04109 Leipzig, Germany.
Neurosci Lett. 2006 Mar 27;396(2):97-101. doi: 10.1016/j.neulet.2005.11.016. Epub 2005 Dec 5.
Ischemia-reperfusion of the rat retina causes gliosis of Müller 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, Müller 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.
大鼠视网膜的缺血再灌注会导致Müller细胞发生胶质增生,这与它们的钾离子电导降低有关。通过使用定量PCR和视网膜切片的免疫组织化学染色,我们研究了短暂缺血再灌注对两种内向整流钾离子(Kir)通道Kir4.1和Kir2.1在视网膜中表达的影响。在对照视网膜中,Müller细胞显著表达Kir4.1和Kir2.1蛋白。再灌注7天后,Kir4.1蛋白的表达强烈下调,而Kir2.1蛋白表达保持不变。缺血后Kir4.1 mRNA的表达降低了55%,而Kir2.1 mRNA的表达未改变。这些数据表明,视网膜缺血后,不同Kir通道的胶质细胞表达受到不同调节,对钾离子和水平衡产生有害影响。