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Originally published In Press as doi:10.1167/iovs.08-2332 on September 20, 2008
 (Investigative Ophthalmology and Visual Science. 2009;50:2359-2367.)
© 2009 by The Association for Research in Vision and Ophthalmology, Inc.
doi:10.1167/iovs.08-2332
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Retinal Gene Expression and Müller Cell Responses after Branch Retinal Vein Occlusion in the Rat

Matus Rehak,1 Margrit Hollborn,1,2 Ianors Iandiev,1,3 Thomas Pannicke,4 Anett Karl,4 Antje Wurm,4 Leon Kohen,1,5 Andreas Reichenbach,4 Peter Wiedemann,1 and Andreas Bringmann1

1From the Department of Ophthalmology and Eye Hospital, the 2Interdisciplinary Center of Clinical Research, the 3Translational Center for Regenerative Medicine, and the 4Paul Flechsig Institute of Brain Research, University of Leipzig, Leipzig, Germany; and the 5Helios Klinikum Aue, Aue, Germany.

PURPOSE. In a rat model of branch retinal vein occlusion (BRVO), changes in gene expression of factors implicated in the development of retinal edema and alterations in the properties of Müller cells were determined.

METHODS. In adult Long-Evans rats, BRVO was induced by laser photocoagulation of retinal veins; untreated eyes served as controls. The mRNA levels of after factors were determined with real-time RT-PCR in the neural retina and retinal pigment epithelium after 1 and 3 days of BRVO: VEGF-A, pigment epithelium-derived factor (PEDF), tissue factor, prothrombin, the potassium channel Kir4.1, and aquaporins 1 and 4. Potassium currents were recorded in isolated Müller cells, and cellular swelling was assessed in retinal slices.

RESULTS. In the neural retina, the expression of VEGF was upregulated within 1 day of BRVO and returned to the control level after 3 days. PEDF was upregulated in the neuroretina and retinal pigment epithelium after 3 days of BRVO. Prothrombin, Kir4.1, and both aquaporins were downregulated in the neuroretina. After BRVO, Müller cells displayed a decrease in their potassium currents and an altered distribution of Kir4.1 protein, an increase in the size of their somata, and cellular swelling under hypoosmotic stress that was not observed in control tissues.

CONCLUSIONS. BRVO results in a rapid transient increase in the expression of VEGF and a delayed increase in the expression of PEDF. The downregulation of Kir4.1 and aquaporins, the mislocation of Kir4.1 protein, and the osmotic swelling of Müller cells may contribute to the development of edema and neuronal degeneration.






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