Retinal Ganglion Cell Death Induced by Retinal Ischemia

Vidal‐Sanz, Manuel; Lafuente, M.P.; Mayor, Sergio; Imperial, J Miralles de; Villegas‐Pérez, María Paz

doi:10.1016/s0039-6257(01)00205-3

Cited by 74 publications

(14 citation statements)

References 17 publications

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“…Supplementing the amino acid taurine has recently proven to be a viable approach for slowing retinal ganglion cell degeneration in multiple animal models (Froger et al, 2012; Froger et al, 2013), as well as improving resistance to hypoxic conditions in retinal cell cultures (Chen et al, 2009). Under ischemic conditions, modulation of adrenergic receptors either by using alpha2-agonists (Lafuente et al, 2001; Vidal-Sanz et al, 2001) or beta-2 antagonists (Chen et al, 2007) has provided neuroprotection for retinal ganglion cells. This neuroprotection has been proposed to arise from the regulation of NMDA receptor-mediated transmission onto retinal ganglion cells, despite the fact that these neurons are relatively insensitive to glutamate and NMDA excitotoxicity (Ullian et al, 2004).…”

Section: Disease: Alterations To Structure and Functionmentioning

confidence: 99%

Functional architecture of the retina: Development and disease

Hoon

Okawa

Santina

et al. 2014

Progress in Retinal and Eye Research

457

385

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Structure and function are highly correlated in the vertebrate retina, a sensory tissue that is organized into cell layers with microcircuits working in parallel and together to encode visual information. All vertebrate retinas share a fundamental plan, comprising five major neuronal cell classes with cell body distributions and connectivity arranged in stereotypic patterns. Conserved features in retinal design have enabled detailed analysis and comparisons of structure, connectivity and function across species. Each species, however, can adopt structural and/or functional retinal specializations, implementing variations to the basic design in order to satisfy unique requirements in visual function. Recent advances in molecular tools, imaging and electrophysiological approaches have greatly facilitated identification of the cellular and molecular mechanisms that establish the fundamental organization of the retina and the specializations of its microcircuits during development. Here, we review advances in our understanding of how these mechanisms act to shape structure and function at the single cell level, to coordinate the assembly of cell populations, and to define their specific circuitry. We also highlight how structure is rearranged and function is disrupted in disease, and discuss current approaches to re-establish the intricate functional architecture of the retina.

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Section: Disease: Alterations To Structure and Functionmentioning

confidence: 99%

Functional architecture of the retina: Development and disease

Hoon

Okawa

Santina

et al. 2014

Progress in Retinal and Eye Research

457

385

View full text Add to dashboard Cite

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“…Experiments using fluorogold to label RGCs following retrograde transport from central injection sites have been a basic staple of glaucoma research in recent years (Danias et al, 2003; Filippopoulos et al, 2006; Mittag et al, 2000; Vidal-Sanz et al, 2001). However, direct comparisons between transported tracers and immune-labeled RGCs underscore that axonal transport is challenged prior to loss of cell bodies.…”

Section: Axonopathy In Glaucomamentioning

confidence: 99%

Critical pathogenic events underlying progression of neurodegeneration in glaucoma

Calkins

2012

Progress in Retinal and Eye Research

266

295

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“…Retinal ischemia-reperfusion (I/R) is a well-established animal model to induce RGC degeneration (Sellés-Navarro et al, 1996; Vidal-Sanz et al, 2001; Hartsock et al, 2016; Liu et al, 2019). This model mimics an acute retinal artery occlusion such as CRAO or RGC death such as glaucoma.…”

Section: Introductionmentioning

confidence: 99%

HIF inhibitor topotecan has a neuroprotective effect in a murine retinal ischemia-reperfusion model

Kunimi

Miwa

Katada

et al. 2019

PeerJ

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Purpose The therapeutic approach for retinal ganglion cell (RGC) degeneration has not been fully established. Recently, it has been reported that hypoxia-inducible factor (HIF) may be involved with retinal neurodegeneration. In this study, we investigated neuroprotective effects of a HIF inhibitor against RGC degeneration induced in a murine model of retinal ischemia-reperfusion (I/R). Methods Eight-weeks-old male C57/BL6J mice were treated with intraperitoneal injection of a HIF inhibitor topotecan (1.25 mg/kg) for 14 days followed by a retinal I/R procedure. Seven days after the I/R injury, the therapeutic effect was evaluated histologically and electrophysiologically. Results The increase of HIF-1α expression and the decrease of retinal thickness and RGC number in I/R were significantly suppressed by administration of topotecan. Impaired visual function in I/R was improved by topotecan evaluated with electroretinogram and visual evoked potentials. Conclusions Topotecan administration suppressed HIF-1a expression and improved RGC survival resulting in a functional protection against retinal I/R. These data indicated that the HIF inhibitor topotecan may have therapeutic potentials for RGC degeneration induced with retinal ischemia or high intraocular pressure.

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Retinal Ganglion Cell Death Induced by Retinal Ischemia

Cited by 74 publications

References 17 publications

Functional architecture of the retina: Development and disease

Functional architecture of the retina: Development and disease

Critical pathogenic events underlying progression of neurodegeneration in glaucoma

HIF inhibitor topotecan has a neuroprotective effect in a murine retinal ischemia-reperfusion model

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