Animal Models of Retinal Disease

Fletcher, Erica L.; Jobling, Andrew I; Vessey, Kirstan A.; Luu, Chi D; Guymer, Robyn H.; Baird, Paul N.

doi:10.1016/b978-0-12-384878-9.00006-6

Cited by 92 publications

(86 citation statements)

References 295 publications

(354 reference statements)

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“…Decline in visual functions, particularly dark adaptation, becomes yet another potential biomarker in monitoring/predicting pathologies leading to AMD (22)(23)(24). Although development of a large number of animal models has helped to advance our understanding of retinal pathobiology and identify specific genetic factors that contribute to photoreceptor degeneration, inflammation, and the biochemistry of many retinal processes, these models all have limitations (25)(26)(27)(28). No one animal model fully recapitulates all the phenotypes of human retinal pathology, and patients with AMD also do not fully resemble each other.…”

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confidence: 99%

Serum levels of lipid metabolites in age‐related macular degeneration

et al. 2015

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Age-related macular degeneration (AMD) is a neurodegenerative disease that causes adult-onset blindness. There are 2 forms of this progressive disease: wet and dry. Currently there is no cure for AMD, but several treatment options have started to emerge making early detection critical for therapeutic success. Analysis of the eyes of Abca4 2/2 Rdh8 2/2 mice that display light-induced retinal degeneration indicates that 11-cis-retinal and docosahexaenoic acid (DHA) levels were significantly decreased as compared with the eyes of control dark-adapted C57BL/6J mice. In addition, exposure to intense light correlated with higher levels of prostaglandin G2 in the eyes of Abca4 2/2 Rdh8 2/2 mice. Intense light exposure also lowered DHA levels in the eyes of wild-type C57BL/6J mice without discernible retinal degeneration. Analysis of human serum from patients with AMD recapitulated these dysregulated DHA levels and revealed dysregulation of arachidonic acid (AA) levels as well (∼32% increase in patients with AMD compared with average levels in healthy individuals). From these observations, we then built a statistical model that included levels of DHA and AA from human serum. This model had a 74% probability of correctly identifying patients with AMD from controls. Addition of a genetic analysis for one of the most prevalent amino acid substitutions in the age-related maculopathy susceptibility 2 gene linked to AMD, Ala 69 →Ser, did not improve the statistical model. Thus, we have characterized a reliable method with the potential to detect AMD without a genetic component, paving the way for a larger-scale clinical evaluation. Our studies on mouse models along with the analysis of human serum suggest that our small molecule-based model may serve as an effective tool to estimate the risk of developing AMD.-Orban, T., Johnson, W. M., Dong, Z., Maeda, T., Maeda, A., Sakai, T., Tsuneoka, H., Mieyal, J. J., Palczewski, K. Serum levels of lipid metabolites in age-related macular degeneration. FASEB J. 29, 4579-4588 (2015). www.fasebj.org

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confidence: 99%

Serum levels of lipid metabolites in age‐related macular degeneration

et al. 2015

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“…In mice, the administration of STZ, supplementation with hypercaloric diet (for 21-26 months), gene mutation (spontaneously) may be a choice for the same purpose [66][67][68][69]. Zebrafish (Danio rerio), a small freshwater fish species which originated in the Ganges River, are currently commonly used as an adequate experimental model to study the genetic, cellular, and molecular mechanisms of various human diseases [70].…”

Section: Diabetic Retinopathy (Dr)mentioning

confidence: 99%

Section: Diabetic Retinopathy (Dr)mentioning

confidence: 99%

“…However, pre-retinal neovascularization, microaneurysms, and intraretinal vascular abnormalities are not detected in these rat models. On the other hand, vascular events in non-proliferative diabetic retinopathy (NPDR) such as loss in the capillaries and their cells such as pericyte in the capillary, and thickening at the basement membrane can be developed in rats with STZ or alloxan induced diabetes after six months from the onset of diabetes [66][67][68][69].In rats, it has been used to provide experimental DR formation via the administration of STZ-all-oxane, supplementation with hypercaloric diet (for seven months), leptin receptor gene mutation (spontaneously). In mice, the administration of STZ, supplementation with hypercaloric diet (for 21-26 months), gene mutation (spontaneously) may be a choice for the same purpose [66][67][68][69].…”

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confidence: 99%

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Experimental Animal Models for Retinal and Choroidal Diseases

Turgut

Karanfil

2017

AOVS

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Experimental animal models have critical importance for the recognition and the management of various retinal and choroidal diseases. To date, they were described for the induction of melanoma and neovascularization of choroid, degenerations, and detachment in the retina, proliferative vitreoretinopathy, diabetic and hypertensive retinopathy, pre-retinal neovascularization, central serous chorioretinopathy, retinopathy of prematurity (ROP) or O 2 induced retinopathy (OIR) and retinoblastoma. The aim of this review is to provide an overview of experimental animal models for retinal and choroidal diseases. To know the most favorite models and animals for these diseases will provide many utilities to the researchers in their experimental studies and thesis. Keywords: Experimental Animal Models for Retinal and Choroidal Diseases 2/10Copyright: ©2017 Turgut et al.primate laser-induced CNV models in rhesus and cynomolgus monkeys have been choiced for preclinical evaluation of n-AMD treatment options [19,21,22,26]. Except for the LFC induced CNV, the sub-retinal NV has been formed in transgenic mice through the increased expression of vascular endothelial growth factor in the retina [23]. Retinal Detachment (RD)The animal RD models are important in the evaluation of the pathogenesis of the disease and new treatment methods in . Many studies have used the mouse as a model to study retinal detachment/reattachment. Mouse eye is a good model for the experimental eye diseases because its manupilation is easy [41][42][43][44]. In animal RD models, manual peeling off the neuroretina from the retina pigment epithelium (RPE) and the subretinal injection of saline, balanced salt solution, phosphatebuffered saline (PBS), hyaluronate or RPE cells have been used to establish an experimental RD in rodent eyes and provide the pathologic features of human . The subretinal injection of sodium hyaluronate has some advantages such as no known ocular toxicity and the long-duration of RD compared to others. The subretinal injection of sodium hyaluronate may performed with a trans-vitreal or a trans-scleral way with the observation of the fundus [28,29,[32][33][34]40]. In the trans-vitreal method, a sub-retinal injector is introduced into the vitreous cavity, a peripheral retinotomy is created, and the sodium hyaluronate is injected into the subretinal space. In this method, two retinal tears are created to increase the risk of retinal hemorrhage. Subretinal hemorrhage or hemorrhage entered underneath the retina is toxic for photoreceptor cells through retinal hypoxia and metabolic impairment due toits diffusion barrier effect, and toxicity due to iron in blood in the detached retina. This induces retinal degeneration and RD [28,29,[32][33][34]40].In trans-scleral method, a 30 G needle with a syringe containing sodium hyaluronate is inserted into the subretinal space through the conjunctiva, sclera, choroid, and RPE following reduction of intraocular pressure (IOP) with an anterior chamber parasenthesis. The sodium hyaluronate is ...

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“…Exciting early results from the use of Adeno-associated virus (AAV) vectors in humans to combat Leber's congenital amaurosis (LCA) (Bainbridge et al, 2008;Maguire et al, 2008), a relatively rare form of congenital blindness, has inspired several groups to employ AAV in a number of ways to combat other genetic diseases. Here, the efforts aimed toward one particular disease, retinitis pigmentosa (RP) (Hartong et al, 2006), will be covered, as there are excellent animal models (Rivas and Vecino, 2009;Fletcher et al, 2011) and it offers some straightforward possibilities to save photoreceptor function and/or photoreceptor cells themselves. Ironically, one of the possibilities is to use optogenetics, rather than gene replacement or knock-down, for restoration of vision (Busskamp and Roska, 2011).…”

Section: Introductionmentioning

confidence: 99%

Emerging Gene Therapies for Retinal Degenerations

Cepko¹

2012

J. Neurosci.

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Animal Models of Retinal Disease

Cited by 92 publications

References 295 publications

Serum levels of lipid metabolites in age‐related macular degeneration

Serum levels of lipid metabolites in age‐related macular degeneration

Experimental Animal Models for Retinal and Choroidal Diseases

Emerging Gene Therapies for Retinal Degenerations

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