Muller Glial Cells in Retinal Disease

被引:330
作者
Bringmann, Andreas
Wiedemann, Peter [1 ,2 ]
机构
[1] Univ Leipzig, Dept Ophthalmol, Fac Med, DE-04103 Leipzig, Germany
[2] Univ Leipzig, Hosp Eye, DE-04103 Leipzig, Germany
关键词
Muller cell; Gliosis; Glutamate toxicity; Antioxidants; Adenosine; Edema; ENDOTHELIAL GROWTH-FACTOR; ISCHEMIC RAT RETINA; ELECTROGENIC GLUTAMATE UPTAKE; FIBRILLARY ACIDIC PROTEIN; CYSTOID MACULAR EDEMA; PROLIFERATIVE DIABETIC-RETINOPATHY; OSMOTIC SWELLING CHARACTERISTICS; INDUCED PHOTORECEPTOR APOPTOSIS; RECEPTOR-MEDIATED STIMULATION; FREE-RADICAL SCAVENGERS;
D O I
10.1159/000328979
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
Virtually all pathogenic stimuli activate Muller cells. Reactive Muller cells exert protective and toxic effects on photoreceptors and neurons. They contribute to oxidative stress and glutamate toxicity due to malfunctions of glutamate uptake and glutathione synthesis. Downregulation of potassium conductance disrupts transcellular potassium and water transport, resulting in neuronal hyperexcitability and edema. Protective effects of reactive Muller cells include upregulation of adenosine 5'-triphosphate (ATP)-degrading ectoenzymes, which enhances the extracellular availability of the neuroprotectant adenosine, abrogation of the osmotic release of ATP, which might protect retinal ganglion cells from apoptosis, and the release of antioxidants and neurotrophic factors. The dedifferentiation of reactive Muller cells to progenitor-like cells might have an impact on future therapeutic approaches. A better understanding of the gliotic mechanisms will be helpful in developing efficient therapeutic strategies aiming at increased protective and regenerative properties and decreased toxicity of reactive Muller cells. Copyright (C) 2011 S. Karger AG, Basel
引用
收藏
页码:1 / 19
页数:19
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