title: Proliferative gliosis causes mislocation and inactivation of inwardly rectifying K(+) (Kir) channels in rabbit retinal glial cells.
abstract: Retinal glial (Müller) cells are proposed to mediate retinal potassium homeostasis predominantly by potassium transport through inwardly rectifying K(+) (Kir) channels. Retinal gliosis is often associated with a decrease in glial potassium conductance. To determine whether this decrease is caused by a downregulation of glial Kir channels, we investigated a rabbit model of proliferative vitreoretinopathy (PVR) which is known to be associated with proliferative gliosis. The membrane conductance of control Müller cells is characterized by large Kir currents whereas Müller cells of PVR retinas displayed an almost total absence of Kir currents. In control tissues, Kir2.1 immunoreactivity is localized in the inner stem processes and endfeet of Müller cells whereas Kir4.1 immunoreactivity is largely confined to the Müller cell endfeet. In PVR retinas, there is a mislocation of Kir channel proteins, with Kir4.1 immunoreactivity detectable in Müller cell fibers throughout the whole retina, and a decrease of immunoreactivity in the cellular endfeet. Real-time PCR analysis revealed no alteration of the Kir4.1 mRNA levels in PVR retinas as compared to the controls but a slight decrease in Kir2.1 mRNA. Western blotting showed no difference in the Kir4.1 protein content between control and PVR retinas. The data suggest that proliferative gliosis in the retina is associated with a functional inactivation of glial Kir channels that is not caused by a downregulation of the channel proteins but is associated with their mislocation in the cell membrane.
authors: Paul Flechsig Institute of Brain Research, University of Leipzig Faculty of Medicine, Jahnallee 59, Leipzig, Germany. elke.ulbricht@medizin.uni-leipzig.de
authors: Elke
authors: E
authors: Ulbricht
authors: Thomas
authors: T
authors: Pannicke
authors: Margrit
authors: M
authors: Hollborn
authors: Maik
authors: M
authors: Raap
authors: Iwona
authors: I
authors: Goczalik
authors: Ianors
authors: I
authors: Iandiev
authors: Wolfgang
authors: W
authors: Härtig
authors: Susann
authors: S
authors: Uhlmann
authors: Peter
authors: P
authors: Wiedemann
authors: Andreas
authors: A
authors: Reichenbach
authors: Andreas
authors: A
authors: Bringmann
authors: Mike
authors: M
authors: Francke
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004594:Electrophysiology; D005260:Female; D015870:Gene Expression; D005911:Gliosis / Q000378:metabolism* / Q000473:pathology; D008297:Male; D009457:Neuroglia / Q000378:metabolism*; D016133:Polymerase Chain Reaction / Q000379:methods; D024661:Potassium Channels, Inwardly Rectifying / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics; D011817:Rabbits; D012160:Retina / Q000378:metabolism* / Q000473:pathology; D018630:Vitreoretinopathy, Proliferative / Q000378:metabolism* / Q000473:pathology; D000098854:Kcnj10 Channel
chemical_list: D000098854:Kcnj10 Channel; C489461:Kir2.1 channel; D024661:Potassium Channels, Inwardly Rectifying; D012333:RNA, Messenger