Early Glial Cell Reactivity in Experimental Retinal Detachment: Effect of Suramin

Uhlmann, Susann; Bringmann, Andreas; Uckermann, Ortrud; Pannicke, Thomas; Weick, Michael; Ulbricht, Elke; Goczalik, Iwona; Reichenbach, Andreas; Wiedemann, Peter; Francke, Mike

doi:10.1167/iovs.03-0183

Cited by 42 publications

(33 citation statements)

References 31 publications

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“…Reactive responses of Mü ller cells occur within 24 h of retinal detachment. Suramin inhibits some of these responses and may provide a therapeutic candidate to limit the detrimental effects of immune cell activation and Mü ller cell gliosis during retinal detachment (Uhlmann et al, 2003).…”

Section: Painmentioning

confidence: 99%

Pathophysiology and Therapeutic Potential of Purinergic Signaling

Burnstock

2006

Pharmacological Reviews

569

519

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Section: Painmentioning

confidence: 99%

Pathophysiology and Therapeutic Potential of Purinergic Signaling

Burnstock

2006

Pharmacological Reviews

569

519

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“…Downregulation of carbonic anhydrase [14,15] and inwardly rectifying potassium (Kir) channels (fig. 1d, 2, 3a, b, d) [23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38] results in disturbances of retinal acid-base, ion and water homeostasis (see below) [7,39]. …”

Section: Müller Cell Gliosismentioning

confidence: 99%

“…Such alterations have been observed in animal models of various retinal diseases, including ischemia-reperfusion, inflammation, diabetic retinopathy, blue-light injury, detachment, vein occlusion and proliferative vitreoretinopathy, as well as in Müller cells from patients with proliferative retinopathies (fig. 5a) [17,18,19,20,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,199]. Ischemia causes a decrease in Kir4.1 (but not Kir2.1) expression (fig.…”

Section: Dysfunctional Retinal Potassium Homeostasismentioning

confidence: 99%

Müller Glial Cells in Retinal Disease

Bringmann¹,

Wiedemann²

2011

Ophthalmologica

Self Cite

358

274

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Virtually all pathogenic stimuli activate Müller cells. Reactive Müller 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 Müller 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 Müller 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 Müller cells.

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“…11,12 Mü ller cells have been shown to react within 15 min of RD, 13 with proliferation and hypertrophy of their processes seen as little as two days postdetachment. 14,15 This abnormal growth leads to their extension into the subretinal space, formation of intraretinal scars, and irregularities within retinal synaptic connections. 14,16,17 Visual recovery also may be hampered by an outgrowth of neurites from second-(bipolar and horizontal cells) and third-order neurons (ganglion cells).…”

Section: Introductionmentioning

confidence: 99%

Amino-acid levels in subretinal and vitreous fluid of patients with retinal detachment

Bertram

Bula

Pulido

et al. 2007

Eye

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Purpose To compare the concentration of amino acids in subretinal and vitreous fluid of patients with primary rhegmatogenous retinal detachment to that of control vitreous. Methods This prospective, observational study measured amino-acid levels in subretinal fluid of patients undergoing scleral buckle placement (n ¼ 20) and vitreous fluid in patients undergoing pars plana vitrectomy (n ¼ 5) for primary retinal detachment. Vitreous fluid from patients undergoing vitrectomy for macular hole (n ¼ 7) or epiretinal membrane (n ¼ 3) served as a control. Subretinal fluid and control vitreous were analysed using high-pressure liquid chromatography. Retinal detachment vitreous was analysed using capillary electrophoresis-laser-induced fluorescence. Results Mean levels of glutamate (27.071.7 lM), aspartate (4.174.0 lM), and glycine (44.1731.0 lM) in subretinal fluid and glutamate (13.4711.9 lM) in the vitreous were significantly elevated in retinal detachment compared to control vitreous. A significant, positive association was observed between levels of aspartate and glutamate in subretinal fluid (Spearman's correlation coefficient: 0.74, Po0.01). Mean arginine levels did not differ significantly between subretinal fluid and control vitreous. Levels of alanine, tyrosine, valine, isoleucine, leucine, and phenylalanine were significantly lower in subretinal fluid compared to control vitreous (all Po0.01). Conclusions Glutamate levels in subretinal fluid and vitreous of patients with primary retinal detachment is significantly elevated in comparison to control vitreous. This finding lends further support to the hypothesis that elevated glutamate levels may result from ischaemia of the outer retina secondary to retinal detachment.

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Early Glial Cell Reactivity in Experimental Retinal Detachment: Effect of Suramin

Cited by 42 publications

References 31 publications

Pathophysiology and Therapeutic Potential of Purinergic Signaling

Pathophysiology and Therapeutic Potential of Purinergic Signaling

Müller Glial Cells in Retinal Disease

Amino-acid levels in subretinal and vitreous fluid of patients with retinal detachment

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