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Citation
Tags
HERO ID
1038771
Reference Type
Journal Article
Subtype
Review
Title
Role of Muller cells in retinal degenerations
Author(s)
Bringmann, A; Reichenbach, A
Year
2001
Is Peer Reviewed?
Yes
Journal
Frontiers in Bioscience
ISSN:
1093-9946
EISSN:
1093-4715
Volume
6
Page Numbers
E72-E92
Language
English
PMID
11578954
Abstract
Muller (radial glial) cells span the entire thickness of the retina, and contact and ensheath every type of neuronal cell body and process. This morphological relationship is reflected by a multitude of functional interactions between retinal neurons and Muller cells, including extracellular ion homeostasis and glutamate recycling by Muller cells. Virtually every disease of the retina is associated with a reactive Muller cell gliosis. Muller cell gliosis may either support the survival of retinal neurons or accelerate the progress of neuronal degeneration. Muller cells are key mediators of nerve cell protection, especially via release of basic fibroblast growth factor, via uptake and degradation of the excitotoxin glutamate, and via secretion of the antioxidant glutathione. Neovascularization during hypoxic conditions is mediated by Muller cells via release of vascular endothelial growth factor and transforming growth factor beta or via direct contact to endothelial cells. Primary Muller cell insufficiency has been suggested to be the cause of different cases of retinal degeneration including hepatic and methanol-induced retinopathy and glaucoma. It is conceivable that, in the future, new therapeutic strategies may utilize Muller cells for, e.g., somatic gene therapy or transdifferentiation of retinal neurons from dedifferentiated Muller cells.
Keywords
Muller cell; glia; reactive gliosis; ionic homeostasis; transmitter recycling; trophic factors; proliferative retinopathies; neovascularization; retina degeneration; ischemia; hepatic retinopathy; retinoschisis; review
Tags
IRIS
•
Methanol (Non-Cancer)
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