scholarly journals Polyethylene Glycol (PEG)-induced Mouse Model of Choroidal Neovascularization

2011 ◽  
Vol 286 (18) ◽  
pp. 16229-16237 ◽  
Author(s):  
Valeriy V. Lyzogubov ◽  
Ruslana G. Tytarenko ◽  
Juan Liu ◽  
Nalini S. Bora ◽  
Puran S. Bora
Keyword(s):  
Mouse Model ◽  
Choroidal Neovascularization ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Basic Fgf ◽  
Age Related ◽  
Complement Component C3 ◽  
The Complement System ◽  
Different Doses

In this study, we describe a new method for inducing choroidal neovascularization (CNV) in C57BL/6 mice, an animal model of wet age-related macular degeneration (AMD). AMD is a disease that causes central blindness in humans. We injected PEG-8 subretinally in different doses (0.125–2 mg) to induce CNV. After PEG-8 injection, we examined CNV at several time points (days 3–42). We also used Western blotting, immunohistochemistry, and ELISA to examine the complement component C3 split products, C9, VEGF, TGF-β2, and basic FGF. As early as day 1 after treatment, we found that a single subretinal injection of 1 mg of PEG-8 increased the C3 split products and the C9, TGF-β2, and basic FGF levels in the retinal pigment epithelium-choroid tissue. By day 3 after PEG-8 injection, the intraocular activation of the complement system caused induction and progression of CNV, including new vessels penetrating the Bruch's membrane. At day 5 after PEG-8 injection, we observed a fully developed CNV and retinal degeneration. Thus, in this study, we present a new, inexpensive, and accelerated mouse model of CNV that may be useful to study AMD.

scholarly journals A Circulating MicroRNA Profile in a Laser-Induced Mouse Model of Choroidal Neovascularization

2020 ◽  
Vol 21 (8) ◽  
pp. 2689 ◽  
Author(s):  
Christina Kiel ◽  
Patricia Berber ◽  
Marcus Karlstetter ◽  
Alexander Aslanidis ◽  
Tobias Strunz ◽  
...  
Keyword(s):  
Mouse Model ◽  
Choroidal Neovascularization ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
In Vitro Assays ◽  
Subretinal Space ◽  
Circulating Microrna ◽  
Age Related

Choroidal neovascularization (CNV) is a pathological process in which aberrant blood vessels invade the subretinal space of the mammalian eye. It is a characteristic feature of the prevalent neovascular age-related macular degeneration (nAMD). Circulating microRNAs (cmiRNAs) are regarded as potentially valuable biomarkers for various age-related diseases, including nAMD. Here, we investigated cmiRNA expression in an established laser-induced CNV mouse model. Upon CNV induction in C57Bl/6 mice, blood-derived cmiRNAs were initially determined globally by RNA next generation sequencing, and the most strongly dysregulated cmiRNAs were independently replicated by quantitative reverse transcription PCR (RT-qPCR) in blood, retinal, and retinal pigment epithelium (RPE)/choroidal tissue. Our findings suggest that two miRNAs, mmu-mir-486a-5p and mmur-mir-92a-3p, are consistently dysregulated during CNV formation. Furthermore, in functional in vitro assays, a significant impact of mmu-mir-486a-5p and mmu-mir-92a-3p on murine microglial cell viability was observed, while mmu-mir-92a-3p also showed an impact on microglial mobility. Taken together, we report a robust dysregulation of two miRNAs in blood and RPE/choroid after laser-induced initiation of CNV lesions in mice, highlighting their potential role in pathology and eventual therapy of CNV-associated complications.

The Effects of Indocyanine Green Dye-Enhanced Photocoagulation on the Blood Flow in the Choriocapillaris and the Choroidal Neovascularization (CNV)

2000 ◽  
Author(s):  
C. von Kerczek ◽  
L. Zhu ◽  
A. Ernest ◽  
C. Eggleton ◽  
L. D. T. Topoleski ◽  
...  
Keyword(s):  
Laser Treatment ◽  
Choroidal Neovascularization ◽  
Vision Loss ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
The United States ◽  
Age Related Macular Degeneration ◽  
Central Vision ◽  
Age Related ◽  
Direct Laser

Abstract Age-related macular degeneration (AMD) is the most common cause of vision loss in patients aged 65 years and older in the United States. In the majority of cases, the loss of central vision is secondary to exudative changes and fibrovascular scarring following choroidal neovascularization (CNV). Prompt laser treatment is recommended [Asrani et al., 1996; Macular Photocoagulation Study Group, 1993; Schneider et al, 1998]. However, direct laser treatment to the entire subfoveal lesion is almost invariably associated with immediate loss of central vision. Loss of central vision may be due to direct damage to foveal photoreceptors and retinal pigment epithelium or from damage to the nerve fiber layer serving foveal function [Han et al., 1988].

Pattern Dystrophies and Choroidal Neovascularization

2017 ◽  
pp. 313-320
Keyword(s):  
Visual Acuity ◽  
Choroidal Neovascularization ◽  
Middle Ages ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Subretinal Fluid ◽  
Age Related Macular Degeneration ◽  
Pattern Dystrophy ◽  
Good Visual Acuity ◽  
Age Related

Pattern dystrophies are hereditary dystrophies that come from retinal pigment epithelium and located in the macula. The diagnosis is usually made around the middle ages. Pigment accumulations in the macula and around the macula, are seen bilaterally and symmetrical in the beginning, are sub-divided depending on pigment scattering pattern. These are adult-onset foveomacular vitelliform dystrophy, butterfly-like pattern dystrophy, reticular pattern dystrophy, and fundus pulverulentus. Usually in patients with pattern dystrophy have good visual acuity, after progression central visual acuity lessens with RPE atrophy or choroidal neovascularization development. In choroidal neovascularization secondary to age-related macular degeneration there is no typical pigmentation in the macula. On the other hand, in choroidal neovascularization related to pattern dystrophy, hemorrhage, and intra/subretinal fluid do not exist. Today choroidal neovascularization prognosis, which is treated with intravitreal anti-VEGF injections, is quite good. At least, one eye of the patients has satisfactory vision. Sometimes, in especially patients with isolated pattern dystrophy, not hereditary, there may be spontaneous regression of choroidal neovascularization.

New Vessel Formation, Choroidal Neovascularization, and Causes

2017 ◽  
pp. 273-279
Keyword(s):  
Retinal Pigment Epithelium ◽  
Macular Degeneration ◽  
Blood Vessels ◽  
Choroidal Neovascularization ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Eye Diseases ◽  
Age Related Macular Degeneration ◽  
Vessel Formation ◽  
Age Related

Choroidal neovascularization is defined as the formation of new blood vessels located between the retinal pigment epithelium and the Bruch's membrane. The neovascular structure is taken origin from the choroid, crosses the Bruch membrane, and affects the photoreceptors with RPE. It is most frequently observed in Age-Related Macular Degeneration and less frequently in other eye diseases. This review mentions choroidal neovascularization and its causes as a general.

scholarly journals Complement System and Potential Therapeutics in Age-Related Macular Degeneration

2021 ◽  
Vol 22 (13) ◽  
pp. 6851
Author(s):  
Young-Gun Park ◽  
Yong-Soo Park ◽  
In-Beom Kim
Keyword(s):  
Macular Degeneration ◽  
Complement System ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Retinal Pigment Epithelium Cell ◽  
Immune Surveillance ◽  
Geographic Atrophy ◽  
Age Related Macular Degeneration ◽  
Age Related ◽  
The Complement System

Age-related macular degeneration (AMD) is a complex multifactorial disease characterized in its late form by neovascularization (wet type) or geographic atrophy of the retinal pigment epithelium cell layer (dry type). The complement system is an intrinsic component of innate immunity. There has been growing evidence that the complement system plays an integral role in maintaining immune surveillance and homeostasis in AMD. Based on the association between the genotypes of complement variants and AMD occurrence and the presence of complement in drusen from AMD patients, the complement system has become a therapeutic target for AMD. However, the mechanism of complement disease propagation in AMD has not been fully understood. This concise review focuses on an overall understanding of the role of the complement system in AMD and its ongoing clinical trials. It provides further insights into a strategy for the treatment of AMD targeting the complement system.

scholarly journals Distinct effects of complement and of NLRP3- and non-NLRP3 inflammasomes for choroidal neovascularization

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Jakob Malsy ◽  
Andrea C Alvarado ◽  
Joseph O Lamontagne ◽  
Karin Strittmatter ◽  
Alexander G Marneros
Keyword(s):  
Choroidal Neovascularization ◽  
Nlrp3 Inflammasome ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Inflammasome Activation ◽  
Rpe Cells ◽  
Age Related ◽  
Nlrp3 Inflammasome Activation ◽  
Nlrp3 Inflammasomes

NLRP3 inflammasome activation and complement-mediated inflammation have been implicated in promoting choroidal neovascularization (CNV) in age-related macular degeneration (AMD), but central questions regarding their contributions to AMD pathogenesis remain unanswered. Key open questions are (1) whether NLRP3 inflammasome activation mainly in retinal pigment epithelium (RPE) or rather in non-RPE cells promotes CNV, (2) whether inflammasome activation in CNV occurs via NLRP3 or also through NLRP3-independent mechanisms, and (3) whether complement activation induces inflammasome activation in CNV. Here we show in a neovascular AMD mouse model that NLRP3 inflammasome activation in non-RPE cells but not in RPE cells promotes CNV. We demonstrate that both NLRP3-dependent and NLRP3-independent inflammasome activation mechanisms induce CNV. Finally, we find that complement and inflammasomes promote CNV through independent mechanisms. Our findings uncover an unexpected role of non-NLRP3 inflammasomes for CNV and suggest that combination therapies targeting inflammasomes and complement may offer synergistic benefits to inhibit CNV.

Sign in / Sign up

Export Citation Format

Share Document