Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9429271 | Neuroscience Letters | 2005 | 6 Pages |
Abstract
Müller cell dysfunction may contribute to the early pathological changes associated with conditions such as diabetes, that cause breakdown of the blood-retinal barrier. In this study we used an in vitro model of the blood-retinal barrier to investigate Müller cell effects on retinal vascular endothelial cell monolayer permeability under normoxic (20% oxygen) and hypoxic (1% oxygen) conditions. Second passage bovine retinal capillary endothelial cells were co-cultured with retinal Müller cells on opposite sides of a 0.4 μm pore size polycarbonate Transwell filter or in medium that was continually conditioned by Müller cells. Permeability changes were observed for up to 24 h of hypoxia by measurement of [3H]-inulin and [14C]-albumin flux across the endothelial cell monolayer. Endothelial cell barrier function was enhanced by co-culturing with Müller cells under normoxic conditions. Under hypoxic conditions however, the barrier was significantly impaired after 12 h of co-culture with Müller cells. These results shed more light on the trophic effect of Müller cells on the blood-retinal barrier, suggesting a critical role in the maintenance and regulation of the barrier in health and during disease.
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Neuroscience
Neuroscience (General)
Authors
Marina Tretiach, Michele C. Madigan, Li Wen, Mark C. Gillies,