Role of Muller cells in retinal degenerations

Muller (radial glial) cells span the entire thickness of the retina, and co ntact and ensheath every type of neuronal cell body and process. This morph ological relationship is reflected by a multitude of functional interaction s between retinal neurons and Muller cells, including extracellular ion hom eostasis and glutamate recycling by Muller cells. Virtually every disease o f the retina is associated with a reactive Muller cell gliosis. Muller cell gliosis may either support the survival of retinal neurons or accelerate t he progress of neuronal degeneration. Muller cells are key mediators of ner ve cell protection, especially via release of basic fibroblast growth facto r, via uptake and degradation of the excitotoxin glutamate, and via secreti on of the antioxidant glutathione. Neovascularization during hypoxic condit ions is mediated by Muller cells via release of vascular endothelial growth factor and transforming growth factor beta or via direct contact to endoth elial cells. Primary Muller cell insufficiency has been suggested to be the cause of different cases of retinal degeneration including hepatic and met hanol-induced retinopathy and glaucoma. It is conceivable that, in the futu re, new therapeutic strategies may utilize Muller cells for, e.g., somatic gene therapy or transdifferentiation of retinal neurons from dedifferentiat ed Muller cells.