Changes in Membrane Conductance Play a Pathogenic Role in Osmotic Glial Cell Swelling in Detached Retinas

Wurm, Antje; Pannicke, Thomas; Iandiev, Ianors; Bühner, Eva; Pietsch, Uta–Carolin; Reichenbach, Andreas; Wiedemann, Peter; Uhlmann, Susann; Bringmann, Andreas

doi:10.2353/ajpath.2006.060628

Cited by 38 publications

(49 citation statements)

References 38 publications

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“…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%

“…6b) [35,138,170,171,172,173,174]. Adenosine cannot be extracellularly generated from ATP because the retinal parenchyma lacks the nucleoside triphosphate diphosphohydrolase (NTPDase) 1 (fig.…”

Section: Extracellular Formation Of Adenosinementioning

confidence: 99%

“…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%

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Müller Glial Cells in Retinal Disease

Bringmann¹,

Wiedemann²

2011

Ophthalmologica

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351

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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Section: Dysfunctional Retinal Potassium Homeostasismentioning

confidence: 99%

Section: Extracellular Formation Of Adenosinementioning

confidence: 99%

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Müller Glial Cells in Retinal Disease

Bringmann¹,

Wiedemann²

2011

Ophthalmologica

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351

274

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“…Previous serial observations of macular holes show that avulsed foveal tissues rapidly decrease in size eventually becoming invisible in OCT. [43][44][45] Regarding foveal photoreceptor degenerative changes, tissue changes at the hole margins are very similar to those in experimental retinal detachment (from ischemia and vitreous humor contact). 46,47 Histologically, INL cystic changes start within 3 days after rhegmatogenous retinal detachment, showing no dye leakage or pooling in fluorescein angiography, 46 and these changes are known to be related with decreased Müller cell water transport functions. With time, photoreceptor degeneration is initiated from electrolyte imbalance and ischemia.…”

Section: Sdmentioning

confidence: 99%

Determination of macular hole size in relation to individual variabilities of fovea morphology

Shin

Chu

Hong

et al. 2015

Eye

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Purpose To determine the preoperative anatomic factors in macular holes and their correlation to hole closure. Methods Forty-six eyes with consecutive unilateral macular hole who had undergone surgery and followed up for at least 6 months were enrolled. Optical coherence tomography images and best-corrected visual acuity (BCVA) within 2 weeks prior to operation and 6 months after surgery were analyzed. The maximal hole dimension, foveal degeneration factors (inner nuclear layer cysts, outer segment (OS) shortening) and the widest foveolar floor size of the fellow eyes were measured. For overcoming preoperative individual variability of foveal morphology, an 'adjusted' hole size parameter (the ratio between the hole size and the fellow eye foveolar floor size) was used based on the fact that both eyes were morphologically symmetrical. Results Mean preoperative BCVA (logMAR) was 1.03 ± 0.43 and the mean postoperative BCVA was 0.50 ± 0.38 at 6 months. Preoperative BCVA is significantly associated with postoperative BCVA (P = 0.0002). The average hole diameter was 448.9 ± 196.8 μm and the average fellow eye foveolar floor size was 461.3 ± 128.4 μm. There was a correlation between hole diameter and the size of the fellow eye foveolar floor (Pearson's coefficient = 0.608, Po0.0001). The adjusted hole size parameter was 0.979 ± 0.358 (0.761-2.336), which was a strong predictor for both anatomic (P = 0.0281) and visual (P = 0.0016) outcome. Conclusion When determining the extent of preoperative hole size, we have to take into consideration the foveal morphologic variations among individuals. Hole size may be related to the original foveal shape, especially in relation to the centrifugal retraction of the foveal tissues.

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“…Briefly, glutamate derived from both Müller cells and neurons and acting at its metabotropic receptors, evokes release of ATP from Müller cells. Ecto-ATPases catabolize ATP to ADP, which activates P2Y 1 , which, in turn, triggers the release of adenosine from Müller cells [111][112][113]. Adenosine then activates A 1 receptors, leading to the opening of potassium and chloride channels in Müller cell membranes and ion efflux compensating the osmotic gradient across the plasma membrane and thus preventing hypo-osmotic swelling.…”

Section: Oligodendrocytesmentioning

confidence: 99%

Purinergic trophic signalling in glial cells: functional effects and modulation of cell proliferation, differentiation, and death

Lecca

Ceruti

Fumagalli

et al. 2012

Purinergic Signalling

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In the last decades, the discovery that glial cells do not only fill in the empty space among neurons or furnish them with trophic support but are rather essential participants to the various activities of the central and peripheral nervous system has fostered the search for the signalling pathways controlling their functions. Since the early 1990s, purines were foreseen as some of the most promising candidate molecules. Originally just a hypothesis, this has become a certainty as experimental evidence accumulated over years, as demonstrated by the exponentially growing number of articles related to the role of extracellular nucleotides and nucleosides in controlling glial cell functions. Indeed, as new functions for already known glial cells (for example, the ability of parenchymal astrocytes to behave as stem cells) or new subtypes of glial cells (for example, NG2 + cells, also called polydendrocytes) are discovered also, new actions and new targets for the purinergic system are identified. Thus, glial purinergic receptors have emerged as new possible pharmacological targets for various acute and chronic pathologies, such as stroke, traumatic brain and spinal cord injury, demyelinating diseases, trigeminal pain and migraine, and retinopathies. In this article, we will summarize the most important and promising actions mediated by extracellular purines and pyrimidines in controlling the functions, survival, and differentiation of the various "classical" types of glial cells (i.e., astrocytes, oligodendrocytes, microglial cells, Müller cells, satellite glial cells, and enteric glial cells) but also of some rather new members of the family (e.g., polydendrocytes) and of other cells somehow related to glial cells (e.g., pericytes and spinal cord ependymal cells).

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Changes in Membrane Conductance Play a Pathogenic Role in Osmotic Glial Cell Swelling in Detached Retinas

Cited by 38 publications

References 38 publications

Müller Glial Cells in Retinal Disease

Müller Glial Cells in Retinal Disease

Determination of macular hole size in relation to individual variabilities of fovea morphology

Purinergic trophic signalling in glial cells: functional effects and modulation of cell proliferation, differentiation, and death

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