Retinal Gene Expression and Müller Cell Responses after Branch Retinal Vein Occlusion in the Rat

Rehák, Matúš; Hollborn, Margrit; Iandiev, Ianors; Pannicke, Thomas; Karl, Anett; Wurm, Antje; Kohen, Leon; Reichenbach, Andreas; Wiedemann, Peter; Bringmann, Andreas

doi:10.1167/iovs.08-2332

Cited by 94 publications

(83 citation statements)

References 30 publications

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“…These changes were probably brought about by hypoxia and decreased nitric oxide production, 39 apoptosis, 40 and general inflammation with alterations in retinal gene expression and Müller cell activity throughout the retina. 41 As expected with retinal ischemia, the inner retinal responses (iN1) were more severely depressed by the BRVO than outer retinal responses (P1).…”

Section: Consequences Of Gdnf Treatment In Brvo Eyessupporting

confidence: 52%

Effect of Glial Cell Line-Derived Neurotrophic Factor on Retinal Function after Experimental Branch Retinal Vein Occlusion

Ejstrup

Cour

Kyhn

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. The objective of the study was to investigate the effect of glial cell line-derived neurotrophic factor (GDNF) on the multifocal electroretinogram (mfERG) following an induced branch retinal vein occlusion (BRVO) in pigs.METHODS. Electrophysiological examination of the retina was performed in 20 pigs with standard and four-frame mfERG 4 weeks after induced BRVO and intravitreal injection of GDNF or vehicle. BRVO was induced by intraocular diathermia of the superior retinal vein. Inner retinal function was measured by analysis of the four-frame mfERG (iN1) and outer retinal function with standard mfERG (P1).RESULTS. In GDNF-treated BRVO eyes, P1 and iN1 amplitudes (P ¼ 0.51 and 0.78) or implicit times (P ¼ 0.08 and 0.99) did not differ from those in healthy fellow eyes. After vehicle injection, P1 and iN1 amplitudes of BRVO eyes were significantly lower than in the healthy fellow eye (P ¼ 0.022 and 0.013). The log ratios of mfERG amplitudes between experimental and healthy fellow eyes were calculated (BRVO/healthy). GDNF improved the ratios of the four-frame mfERG CONCLUSIONS. GDNF appears neuroprotective on retinal electrophysiological function after BRVO. The efficacy and safety of GDNF remain to be investigated in primate eyes. (Invest Ophthalmol Vis Sci. 2012;53:6207-6213)

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Section: Consequences Of Gdnf Treatment In Brvo Eyessupporting

confidence: 52%

Effect of Glial Cell Line-Derived Neurotrophic Factor on Retinal Function after Experimental Branch Retinal Vein Occlusion

Ejstrup

Cour

Kyhn

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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“…Creating retinal occlusions has depended primarily upon the slit-lamp biomicroscope [3][4][5][6][7][8][9]. Our multimodal imaging system for producing retinal occlusions in animal models has several advantages over using a slit-lamp biomicroscope.…”

Section: Discussionmentioning

confidence: 99%

“…In the first technique, the fundus is visualized with a modified slit-lamp biomicroscope using a high-power laser delivery system (~100-200 mW) [3][4][5]. A skilled operator then manually delivers high energy laser shots to a target retinal vessel until vascular occlusion appears to have occurred.…”

Section: Introductionmentioning

confidence: 99%

Optical coherence tomography angiography of retinal vascular occlusions produced by imaging-guided laser photocoagulation

Soetikno

Xiao

Liu

et al. 2017

Biomed. Opt. Express

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Abstract:Retinal vascular occlusive diseases represent a major form of vision loss worldwide. Rodent models of these diseases have traditionally relied upon a slit-lamp biomicroscope to help visualize the fundus and subsequently aid delivery of high-power laser shots to a target vessel. Here we describe a multimodal imaging system that can produce, image, and monitor retinal vascular occlusions in rodents. The system combines a spectraldomain optical coherence tomography system for cross-sectional structural imaging and three-dimensional angiography, and a fluorescence scanning laser ophthalmoscope for Rose Bengal monitoring and high-power laser delivery to a target vessel. This multimodal system facilitates the precise production of occlusions in the branched retinal veins, central retinal vein, and branched retinal arteries. Additionally, changes in the retinal morphology and retinal vasculature can be longitudinally documented. With our device, retinal vascular occlusions can be easily and consistently created, which paves the way for futures studies on their pathophysiology and therapeutic targets.

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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

292

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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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Retinal Gene Expression and Müller Cell Responses after Branch Retinal Vein Occlusion in the Rat

Cited by 94 publications

References 30 publications

Effect of Glial Cell Line-Derived Neurotrophic Factor on Retinal Function after Experimental Branch Retinal Vein Occlusion

Effect of Glial Cell Line-Derived Neurotrophic Factor on Retinal Function after Experimental Branch Retinal Vein Occlusion

Optical coherence tomography angiography of retinal vascular occlusions produced by imaging-guided laser photocoagulation

Müller Glial Cells in Retinal Disease

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