| |
107. DOG-Kongress Home
DOG-Kongressinformation
DOG-Kongress Bildergalerie
Grußworte
Organisation, Termine
Ablauf des Kongresses
Preise und Forschungsförderungen
Höhepunkte
Wissenschaftliches Programm
Feierliche Eröffnung
Schwerpunkte
Wissenschaftliches Programm
- Do, 24.09.09
- Fr, 25.09.09
- Sa, 26.09.09
- So, 27.09.09
- Posterausstellung
Symposien
Kurse
Firmenveranstaltungen
Satellitenprogramm
Hinweise, Informationen
Rahmenprogramm
Sponsoren, Industrie
Presseservice
Programm downloaden / drucken [PDF, 11 MB]
Vorprogramm downloaden / drucken [PDF, 3 MB]
DOG-Homepage
|
|
Abstract
DO.09.06
Role of Müller cells in retinal edema
Andreas Bringmann
Klinik und Poliklinik für Augenheilkunde, Universitätsklinikum Leipzig, Leipzig
Background
Macular edema is a major cause of vision loss. In addition to vascular leakage, dysfunctional fluid clearance mechanisms are suggested to be required for the development of retinal edema. Normally, Müller cells clear excess fluid from the retinal tissue, in part by water transport osmotically coupled to potassium currents. A dysfunction of the fluid clearance by Müller cells may contribute to the development of cytotoxic edema which is characterized by cellular swelling. We investigated whether the osmotic swelling characteristics of Müller cells is altered in animal models of various retinopathies.
Methods
Rat models of retinal ischemia-reperfusion, ocular inflammation, diabetes and blue light-induced retinal damage were investigated. The osmotic swelling of Müller cell bodies was examined in freshly isolated retinal slices. Potassium currents were recorded in isolated Müller cells.
Results
We found that Müller cells in tissue slices of pathologically altered retinas displayed cellular swelling during superfusion with a hypoosmolar solution whereas cells of control retinas did not swell under such conditions. The swelling of Müller cells reflects an alteration in the water transport through the cells. The induction of osmotic swelling was associated with a functional inactivation of potassium channels in Müller cells and caused by factors which are known to contribute to retinal edema formation such as oxidative stress and inflammatory factors like prostaglandins. The anti-inflammatory steroid triamcinolone acetonide, which is used clinically for the rapid resolution of retinal edema, prevented the osmotic swelling of Müller cells by activation of endogenous adenosine signaling. Triamcinolone stimulated the release of adenosine from the retinal tissue which activated adenosine A1 receptors resulting in the opening of potassium channels in the Müller cell membrane.
Conclusions
Impaired fluid clearance normally carried out by Müller cells may result in cytotoxic edema characterized by intracellular water accumulation. We suggest that triamcinolone stimulates the fluid absorption from the retinal tissue because the opening of potassium channels in Müller cell membranes improves the transport of osmolytes and, thus, of water through the cells. |
|