Topical Treatment With Bromfenac Reduces Retinal Gliosis and Inflammation After Optic Nerve Crush

Rovere, Giuseppe; Nadal-Nicolás, Francisco M.; Sobrado‐Calvo, Paloma; García‐Bernal, David; Villegas‐Pérez, María Paz; Vidal‐Sanz, Manuel; Agudo‐Barriuso, Marta

doi:10.1167/iovs.16-20425

Cited by 17 publications

(15 citation statements)

References 59 publications

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“…The first phase, in contrast with axotomy or LP-OHT, is very quick so that by day 3 approximately 65% Brn3a + RGCs are lost (Rovere et al, 2016b). Thereafter RGC loss progressed further to 70% by 14 days and to 87% by 45 days, but, as it occurs after LP-OHT, their survival percentage is higher than after axotomy (e.g., 13% at 45 days vs. the 5% found after ONT).…”

Section: Resultsmentioning

confidence: 99%

“…This RNFL swelling could be explained by an alteration of the axoplasmic transport (McKerracher et al, 1990; Pease et al, 2000), or by an inflammatory response that includes macro and microglial proliferation in the RNFL (Salvador-Silva et al, 2000; Sobrado-Calvo et al, 2007; Ramirez et al, 2010; De Hoz et al, 2013; Galindo-Romero et al, 2013b; Rojas et al, 2014). Indeed, a recent study has shown that administration of non-steroidal anti-inflammatory drugs results in a decrease of the RNFL swelling that follows ONT (Rovere et al, 2016b). …”

Section: Resultsmentioning

confidence: 99%

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Shared and Differential Retinal Responses against Optic Nerve Injury and Ocular Hypertension

et al. 2017

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Glaucoma, one of the leading causes of blindness worldwide, affects primarily retinal ganglion cells (RGCs) and their axons. The pathophysiology of glaucoma is not fully understood, but it is currently believed that damage to RGC axons at the optic nerve head plays a major role. Rodent models to study glaucoma include those that mimic either ocular hypertension or optic nerve injury. Here we review the anatomical loss of the general population of RGCs (that express Brn3a; Brn3a+RGCs) and of the intrinsically photosensitive RGCs (that express melanopsin; m+RGCs) after chronic (LP-OHT) or acute (A-OHT) ocular hypertension and after complete intraorbital optic nerve transection (ONT) or crush (ONC). Our studies show that all of these insults trigger RGC death. Compared to Brn3a+RGCs, m+RGCs are more resilient to ONT, ONC, and A-OHT but not to LP-OHT. There are differences in the course of RGC loss both between these RGC types and among injuries. An important difference between the damage caused by ocular hypertension or optic nerve injury appears in the outer retina. Both axotomy and LP-OHT induce selective loss of RGCs but LP-OHT also induces a protracted loss of cone photoreceptors. This review outlines our current understanding of the anatomical changes occurring in rodent models of glaucoma and discusses the advantages of each one and their translational value.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Shared and Differential Retinal Responses against Optic Nerve Injury and Ocular Hypertension

et al. 2017

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“…4 Such gliosis might interfere with detection of GCC thinning by SD-OCT. Transsynaptic degeneration from post-geniculate neurologic disease is generally not associated with retinal gliosis.…”

Section: Discussionmentioning

confidence: 99%

Progression of transsynaptic retinal degeneration with spectral-domain optical coherence tomography

Schwartz

Monroig

Flynn

2017

American Journal of Ophthalmology Case Reports

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Purpose To illustrate the progression of retrograde transsynaptic retinal degeneration using spectral- domain optical coherence tomography (SD-OCT). Observations A 60 year-old man with a stroke was followed over a 17-month period using SD-OCT of the macula, ganglion cell layer (GCC), and retinal nerve fiber layer. Transsynaptic retinal degeneration progressed over this time. Conclusions and Importance Retrograde transsynaptic retinal degeneration may occur in patients with homonymous visual field loss caused by post-geniculate neurologic disease. This is best detected as homonymous thinning of the retina, corresponding to the pattern of visual field loss, using SD-OCT of the GCC and macula. The retinal changes occur at a variable time following the onset of neurologic disease.

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“…Among rodent models of glaucoma, the optic nerve crush (ONC) model that mimics the IOP-induced compression at the ON head [5], is used to induce a rapid degeneration of RGC axons and an acute RGC injury, eventually leading to RGC death with relatively little inter-animal variability [6]. The mechanism of RGC death after ONC is not fully understood, although inflammatory events triggered by ON damage seem to play a major role [7]. In the inflammatory response, activated glial cells surrounding RGCs are characterized by the phosphorylation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), a critical regulator of inflammatory processes, which leads to increased expression of inflammatory cytokines as demonstrated in DBA/2J mice, a model of inherited glaucoma [8].…”

Section: Introductionmentioning

confidence: 99%

Protective Efficacy of a Dietary Supplement Based on Forskolin, Homotaurine, Spearmint Extract, and Group B Vitamins in a Mouse Model of Optic Nerve Injury

et al. 2019

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Glaucoma is a multifactorial blinding disease with a major inflammatory component ultimately leading to apoptotic retinal ganglion cell (RGC) death. Pharmacological treatments lowering intraocular pressure can help slow or prevent vision loss although the damage caused by glaucoma cannot be reversed. Recently, nutritional approaches have been evaluated for their efficacy in preventing degenerative events in the retina although mechanisms underlying their effectiveness remain to be elucidated. Here, we evaluated the efficacy of a diet supplement consisting of forskolin, homotaurine, spearmint extract, and vitamins of the B group in counteracting retinal dysfunction in a mouse model of optic nerve crush (ONC) used as an in vivo model of glaucoma. After demonstrating that ONC did not affect retinal vasculature by fluorescein angiography, we determined the effect of the diet supplement on the photopic negative response (PhNR) whose amplitude is strictly related to RGC integrity and is therefore drastically reduced in concomitance with RGC death. We found that the diet supplementation prevents the reduction of PhNR amplitude (p < 0.001) and concomitantly counteracts RGC death, as in supplemented mice, RGC number assessed immunohistochemically is significantly higher than that in non-supplemented animals (p < 0.01). Major determinants of the protective efficacy of the compound are due to a reduction of ONC-associated cytokine secretion leading to decreased levels of apoptotic markers that in supplemented mice are significantly lower than in non-supplemented animals (p < 0.001), ultimately causing RGC survival and ameliorated visual dysfunction. Overall, our data suggest that the above association of compounds plays a neuroprotective role in this mouse model of glaucoma thus offering a new perspective in inflammation-associated neurodegenerative diseases of the inner retina.

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Topical Treatment With Bromfenac Reduces Retinal Gliosis and Inflammation After Optic Nerve Crush

Cited by 17 publications

References 59 publications

Shared and Differential Retinal Responses against Optic Nerve Injury and Ocular Hypertension

Shared and Differential Retinal Responses against Optic Nerve Injury and Ocular Hypertension

Progression of transsynaptic retinal degeneration with spectral-domain optical coherence tomography

Protective Efficacy of a Dietary Supplement Based on Forskolin, Homotaurine, Spearmint Extract, and Group B Vitamins in a Mouse Model of Optic Nerve Injury

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