Differential regulation of Kir4.1 and Kir2.1 expression in the ischemic rat retina

被引：42

作者：

Iandiev, I

Tenckhoff, S

Pannicke, T

Biedermann, B

Hollborn, M

Wiedemann, P

Reichenbach, A

Bringmann, A

机构：

[1] Univ Leipzig, Fac Med, Dept Ophthalmol, D-04103 Leipzig, Germany

[2] Univ Leipzig, Fac Med, Eye Clin, D-04103 Leipzig, Germany

[3] Univ Leipzig, Fac Med, Paul Flechsig Inst Brain Res, D-04109 Leipzig, Germany

[4] Univ Leipzig, Fac Med, IZKF, D-04109 Leipzig, Germany

来源：

NEUROSCIENCE LETTERS | 2006年 / 396卷 / 02期

关键词：

retina; glia; Muller cell; potassium channels; RT-PCR; ischemia;

D O I：

10.1016/j.neulet.2005.11.016

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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.

引用

页码：97 / 101

页数：5

共 19 条

[1] Dystrophin Dp71 is critical for the clustered localization of potassium channels in retinal glial cells [J].