Localization of glial aquaporin-4 and Kir4.1 in the light-injured murine retina.
Excessive light causes damage to photoreceptor and pigment epithelial cells, and a local edema in the outer retina. Since Müller glial cells normally mediate the osmohomeostasis in the inner retina (mainly via channel-mediated transport of potassium and water), we determined whether retinal light injury causes an alteration in the retinal localization of glial water (aquaporin-4) and potassium (Kir4.1) channels, and in the potassium conductance of Müller cells. Mice were treated with bright white light (intensity, 15,000lx) for 2h. Light treatment results in Müller cell gliosis as indicated by the enhanced staining of the glial fibrillary acidic protein and an increase in the cell membrane area reflecting cellular hypertrophy. In light-injured retinas, the immunostaining of the photoreceptor water channel aquaporin-1 disappeared along with the degeneration of the outer retina, and the outer nuclear layer contained large spherical bodies representing photoreceptor nuclei which were fused together. The immunostainings of the aquaporin-4 and Kir4.1 proteins were increased in the outer retina after light treatment. Since the amplitude of the potassium currents of Müller cells remained largely unaltered, the increase in the Kir4.1 immunostaining is supposed to be caused by a redistribution of the channel protein. The data indicate that Müller glial cells respond to excessive light with an alteration in the localization of Kir4.1 and aquaporin-4 proteins; this alteration is thought to be a response to the edema in the outer retina and may support the resolution of edema.
Iandiev
Ianors
I
Department of Ophthalmology and Eye Hospital, University of Leipzig Faculty of Medicine, Liebigstr. 10-14, D-04103 Leipzig, Germany.
Pannicke
Thomas
T
Hollborn
Margrit
M
Wiedemann
Peter
P
Reichenbach
Andreas
A
Grimm
Christian
C
Remé
Charlotte E
CE
Bringmann
Andreas
A
D000818:Animals; D051401:Aquaporin 4 / Q000378:metabolism*; D002462:Cell Membrane / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects; D002463:Cell Membrane Permeability / Q000502:physiology / Q000528:radiation effects; D002478:Cells, Cultured; D004487:Edema / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism / Q000528:radiation effects; D005911:Gliosis / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D006984:Hypertrophy / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D008027:Light / Q000009:adverse effects; D051379:Mice; D009457:Neuroglia / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects*; D010786:Photoreceptor Cells / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism*; D020127:Recovery of Function / Q000502:physiology / Q000528:radiation effects; D012160:Retina / Q000378:metabolism / Q000503:physiopathology / Q000528:radiation effects*; D012162:Retinal Degeneration / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D014785:Vision, Ocular / Q000502:physiology / Q000528:radiation effects; D000098854:Kcnj10 Channel
C496031:Aqp4 protein, mouse; D051401:Aquaporin 4; D005904:Glial Fibrillary Acidic Protein; D000098854:Kcnj10 Channel; D024661:Potassium Channels, Inwardly Rectifying