Differential regulation of Kir4.1 and Kir2.1 expression in the ischemic rat retina.
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.
Iandiev
Ianors
I
Paul Flechsig Institute of Brain Research, University of Leipzig Medical Faculty, Jahnallee 59, 04109 Leipzig, Germany.
Tenckhoff
Solveig
S
Pannicke
Thomas
T
Biedermann
Bernd
B
Hollborn
Margrit
M
Wiedemann
Peter
P
Reichenbach
Andreas
A
Bringmann
Andreas
A
D000818:Animals; D002478:Cells, Cultured; D005786:Gene Expression Regulation; D007511:Ischemia / Q000378:metabolism*; D009457:Neuroglia / Q000378:metabolism*; D018917:Optic Neuropathy, Ischemic; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism*; D051381:Rats; D020318:Rats, Long-Evans; D012160:Retina / Q000378:metabolism*; D012171:Retinal Vessels / Q000378:metabolism; D014018:Tissue Distribution; D000098854:Kcnj10 Channel
D000098854:Kcnj10 Channel; C489461:Kir2.1 channel; D024661:Potassium Channels, Inwardly Rectifying