Retinol and retinyl esters in pigment epithelium of rats with inherited retinal degeneration

1976 ◽  
Vol 32 (2) ◽  
pp. 147-148 ◽  
Author(s):  
C. Nicotra ◽  
M. A. Livrea ◽  
F. Cacioppa
Keyword(s):  
Retinal Degeneration ◽  
Pigment Epithelium ◽  
Retinyl Esters ◽  
Inherited Retinal Degeneration

scholarly journals Ccr2 suppression by minocycline in Cx3cr1/Ccr2-visualized inherited retinal degeneration

2020 ◽  
Author(s):  
Ryo Terauchi ◽  
Hideo Kohno ◽  
Sumiko Watanabe ◽  
Saburo Saito ◽  
Akira Watanabe ◽  
...  
Keyword(s):  
Retinal Degeneration ◽  
Expression Pattern ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Rescue Effect ◽  
Ccr2 Expression ◽  
Retinal Inflammation ◽  
Inherited Retinal Degeneration ◽  
Old Mice ◽  
Cx3cr1 Expression

AbstractRetinal inflammation accelerates photoreceptor cell death (PCD) caused by retinal degeneration. Minocycline, a semisynthetic broad-spectrum tetracycline antibiotic, has previously been reported to show PCD rescue effect in retinal degeneration. The purpose of this study was to assess the effect of minocycline on Cx3cr1 and Ccr2 expression in retinal degeneration. Mertk-/-Cx3cr1GFP/+Ccr2RFP/+ mice, which enabled observation of Cx3cr1- and Ccr2-expression pattern in inherited retinal degeneration, were used to test the effect of minocycline. Minocycline was systemically administered to Mertk-/-Cx3cr1GFP/+Ccr2RFP/+ mice. For observing the effect of minocycline on Cx3cr1 and Ccr2 expression, administration was started on 4-week-old mice and continued for 2 weeks. To assess the PCD rescue effect, minocycline was administered to 6-week-old mice for 2 weeks. The expression pattern of Cx3cr1-GFP and Ccr2-RFP were observed on retinal and retinal pigment epithelium (RPE) flat-mounts. The severity of retinal degeneration was assessed on retinal sections. Minocycline administration suppressed Ccr2 expression in Mertk-/-Cx3cr1GFP/+Ccr2RFP/+ mice as observed in retinal and RPE flat-mounts. On the contrary, Cx3cr1 expression was not affected by minocycline administration. Retinal degeneration is ameliorated in minocycline administered Mertk-/-Cx3cr1GFP/+Ccr2RFP/+ mice. In conclusions, Minocycline suppression of Ccr2 expression correlates to amelioration of retinal degeneration.

scholarly journals Study of the functional integrity of the retinal pigment epithelium with a new technique in two models of inherited retinal degeneration

2019 ◽  
Vol 97 (S263) ◽  
Author(s):  
Johnny Di Pierdomenico ◽  
Francisco Javier Valiente Soriano ◽  
Manuel Salinas Navarro ◽  
Diego García‐Ayuso ◽  
María Paz Villegas‐Pérez ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Retinal Degeneration ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
New Technique ◽  
Functional Integrity ◽  
A New Technique ◽  
Inherited Retinal Degeneration

Assessment of inner retinal oxygen metrics and thickness in a mouse model of inherited retinal degeneration

2021 ◽  
Vol 205 ◽  
pp. 108480
Author(s):  
Mansour Rahimi ◽  
Sophie Leahy ◽  
Nathanael Matei ◽  
Norman P. Blair ◽  
Shinwu Jeong ◽  
...  
Keyword(s):  
Mouse Model ◽  
Retinal Degeneration ◽  
Inherited Retinal Degeneration

Neurochemical studies on the inherited retinal degeneration of the rat

1963 ◽  
Vol 3 (7-8) ◽  
pp. 271-280 ◽  
Author(s):  
Vincenzo Bonavita ◽  
Francesco Ponte ◽  
Giuseppe Amore
Keyword(s):  
Retinal Degeneration ◽  
Inherited Retinal Degeneration

Features of local expression of mRNA, IL-1 ß, IL-18, CCL2/MCP-1 in modeling pigment epithelium atrophy and retinal degeneration in the experiment on rabbits

2021 ◽  
Vol 19 (2) ◽  
pp. 54-62
Author(s):  
Vladimir Vladimirovich Neroev ◽  
Natalya Vladimirovna Balatskaya ◽  
Elena Victorovna Svetlova ◽  
Natalia Vladimirovna Neroeva ◽  
Marina Vladimirovna Ryabina ◽  
...  
Keyword(s):  
Retinal Degeneration ◽  
Pigment Epithelium ◽  
Local Expression

scholarly journals Potential Treatment of Retinal Diseases with Iron Chelators

2018 ◽  
Vol 11 (4) ◽  
pp. 112 ◽  
Author(s):  
Wanting Shu ◽  
Joshua Dunaief
Keyword(s):  
Retinal Degeneration ◽  
Therapeutic Potential ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
The Body ◽  
Age Related Macular Degeneration ◽  
Hereditary Diseases ◽  
Iron Chelators ◽  
Excess Iron ◽  
Age Related

Iron is essential for life, while excess iron can be toxic. Iron generates hydroxyl radical, which is the most reactive free radical, causing oxidative stress. Since iron is absorbed through the diet but not excreted from the body, it accumulates with age in tissues, including the retina, consequently leading to age-related toxicity. This accumulation is further promoted by inflammation. Hereditary diseases such as aceruloplasminemia, Friedreich’s ataxia, pantothenate kinase-associated neurodegeneration, and posterior column ataxia with retinitis pigmentosa involve retinal degeneration associated with iron dysregulation. In addition to hereditary causes, dietary or parenteral iron supplementation has been recently reported to elevate iron levels in the retinal pigment epithelium (RPE) and promote retinal degeneration. Ocular siderosis from intraocular foreign bodies or subretinal hemorrhage can also lead to retinopathy. Evidence from mice and humans suggests that iron toxicity may contribute to age-related macular degeneration pathogenesis. Iron chelators can protect photoreceptors and RPE in various mouse models. The therapeutic potential for iron chelators is under investigation.

scholarly journals CRISPR-Cas9 genome engineering: Treating inherited retinal degeneration

2018 ◽  
Vol 65 ◽  
pp. 28-49 ◽  
Author(s):  
Erin R. Burnight ◽  
Joseph C. Giacalone ◽  
Jessica A. Cooke ◽  
Jessica R. Thompson ◽  
Laura R. Bohrer ◽  
...  
Keyword(s):  
Retinal Degeneration ◽  
Genome Engineering ◽  
Inherited Retinal Degeneration

scholarly journals Increased proteasomal activity supports photoreceptor survival in inherited retinal degeneration

2018 ◽  
Vol 9 (1) ◽  
Author(s):  
Ekaterina S. Lobanova ◽  
Stella Finkelstein ◽  
Jing Li ◽  
Amanda M. Travis ◽  
Ying Hao ◽  
...  
Keyword(s):  
Retinal Degeneration ◽  
Proteasomal Activity ◽  
Inherited Retinal Degeneration
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