The retinal pigment epithelium and photoreceptor cells light-and electron microscopic studies on monkey eyes

1975 ◽  
Vol 161 (4) ◽  
Author(s):  
Niels B�low
Keyword(s):  
Retinal Pigment Epithelium ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Photoreceptor Cells ◽  
Electron Microscopic ◽  
Microscopic Studies

JAM-C maintains VEGR2 expression to promote retinal pigment epithelium cell survival under oxidative stress

2017 ◽  
Vol 117 (04) ◽  
pp. 750-757
Author(s):  
Xin Jia ◽  
Chen Zhao ◽  
Qishan Chen ◽  
Yuxiang Du ◽  
Lijuan Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Retinal Pigment Epithelium ◽  
Cell Survival ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Retinal Pigment Epithelium Cell ◽  
Photoreceptor Cells ◽  
Rpe Cells

SummaryJunctional adhesion molecule-C (JAM-C) has been shown to play critical roles during development and in immune responses. However, its role in adult eyes under oxidative stress remains poorly understood. Here, we report that JAM-C is abundantly expressed in adult mouse retinae and choroids in vivo and in cultured retinal pigment epithelium (RPE) and photoreceptor cells in vitro. Importantly, both JAM-C expression and its membrane localisation are downregulated by H2O2-induced oxidative stress. Under H2O2-induced oxidative stress, JAM-C is critically required for the survival of human RPE cells. Indeed, loss of JAM-C by siRNA knockdown decreased RPE cell survival. Mechanistically, we show that JAM-C is required to maintain VEGFR2 expression in RPE cells, and VEGFR2 plays an important role in keeping the RPE cells viable since overexpression of VEGFR2 partially restored impaired RPE survival caused by JAM-C knockdown and increased RPE survival. We further show that JAM-C regulates VEGFR2 expression and, in turn, modulates p38 phosphorylation. Together, our data demonstrate that JAM-C plays an important role in maintaining VEGR2 expression to promote RPE cell survival under oxidative stress. Given the vital importance of RPE in the eye, approaches that can modulate JAM-C expression may have therapeutic values in treating diseases with impaired RPE survival.

The effects of intravitreally injected bevacizumab on the retina and retina pigment epithelium: experimental in-vivo electron microscopic study in intact versus vitrectomized eyes

Open Medicine ◽  
2010 ◽  
Vol 5 (6) ◽  
pp. 745-751 ◽  
Author(s):  
Nilufer Kocak ◽  
Candan Ozogul ◽  
Suleyman Kaynak ◽  
Ulker Sonmez ◽  
Mehmet Zengin ◽  
...  
Keyword(s):  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Intravitreal Bevacizumab ◽  
Electron Microscopic Examination ◽  
Photoreceptor Cells ◽  
Control Group ◽  
Electron Microscopic ◽  
Tissue Samples ◽  
Electron Microscopes

AbstractTo analyze the retinal toxicity of bevacizumab at various doses both in vitrectomized and non-vitrectomized rabbit models. Twenty- eight rabbits were included in the study. Twenty- four rabbits were assigned to six groups, with 4 of the rabbits in the control group. The animals in Groups 1, 2 and 3 received bevacizumab at a dose of 0.3 mg, 0.5 mg and 1.5 mg /eye, respectively. The rabbits in Groups 4, 5 and 6 received intravitreal bevacizumab of 0.3 mg, 0.5 mg and 1.5mg/eye, respectively, after gas compression vitrectomy. Two weeks after the procedure, the rabbits were euthanized. Retina tissue samples were then obtained and examined with both light and electron microscopes. In Groups 1, 2 and 3 after bevacizumab injection, toxic degeneration in the photoreceptor and retinal pigment epithelium cells was observed via electron microscopic examination. The findings in Groups 4 and 5 were normal as compared to the control group. In Group 6, toxicity in the bipolar neurons and photoreceptor cells was noticed. Increased toxicity and retinal penetration were noticed in all administered doses of bevacizumab in the presence of vitreous. In addition, ocular toxicity occurred through the injection of the highest dose of bevacizumab after vitrectomy. It is possible that the bevacizumab dose and the, vitreous are as important as the drug half-life in the vitreous.

scholarly journals UNC569-induced Morphological Changes in Pigment Epithelia and Photoreceptor Cells in the Retina through MerTK Inhibition in Mice

2018 ◽  
Vol 46 (2) ◽  
pp. 193-201 ◽  
Author(s):  
Ayako Sayama ◽  
Keiko Okado ◽  
Koichi Nakamura ◽  
Tatsuya Kawaguchi ◽  
Takuma Iguchi ◽  
...  
Keyword(s):  
Tissue Sample ◽  
Morphological Changes ◽  
Pigment Epithelium ◽  
Outer Nuclear Layer ◽  
Retinal Pigment ◽  
Electron Microscopic Examination ◽  
Photoreceptor Cells ◽  
Electron Microscopic ◽  
Drug Induced ◽  
Photoreceptor Outer Segments

Mer proto-oncogene tyrosine kinase (MerTK), which is expressed in the retinal pigment epithelium (RPE), regulates phagocytosis of shed photoreceptor outer segments (POS). To investigate the effects of drug-induced MerTK inhibition on the retina, UNC569, a specific MerTK inhibitor, was orally administered to male mice at a concentration of 60, 100, or 150 mg/kg for up to 14 days. Furthermore, MerTK inhibition in the retinal tissue sample was examined using a phosphorylation assay following a single dose of UNC569 at 100 mg/kg. In electron microscopic examination, UNC569 at 100 mg/kg or more increased phagosomes and phagolysosomes in the RPE. In addition, UNC569 at 150 mg/kg increased chromatin-condensed nuclei in the outer nuclear layer, indicating the early phase of apoptosis of photoreceptor cells. MiR-183, miR-96, and miR-124, which are enriched in photoreceptor cells, were elevated in the plasma of mice following treatment of 150-mg/kg UNC569, in conjunction with the photoreceptor lesion. Additionally, 100-mg/kg UNC569 inhibited MerTK phosphorylation in the retina. These results suggest that MerTK inhibition impaired phagocytic function of the retina, leading to accumulation of shed POS within the POS layer and increasing phagosomes and phagolysosomes in the RPE to delay POS renewal, resulting in apoptosis of photoreceptor cells.

Pathways for the uptake and conservation of docosahexaenoic acid in photoreceptors and synapses: biochemical and autoradiographic studies

1993 ◽  
Vol 71 (9) ◽  
pp. 690-698 ◽  
Author(s):  
Nicolas G. Bazan ◽  
Elena B. Rodriguez de Turco ◽  
William C. Gordon
Keyword(s):  
Fatty Acid ◽  
Retinal Pigment Epithelium ◽  
Docosahexaenoic Acid ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Photoreceptor Cells ◽  
Plasma Lipoproteins ◽  
Rod Photoreceptor ◽  
Excitable Membranes ◽  
The Central Nervous System

Docosahexaenoic acid (22:6n−3) esterified into phospholipids represents by far the most prevalent fatty acid of rod photoreceptor disc membranes and synaptic terminals. During synaptogenesis and photoreceptor biogenesis, plasma lipoproteins, secreted mainly by the liver, are the main source of plasma 22:6n−3 for the central nervous system. This systemic route (the long loop) also operates in mature animals for morphogenesis and maintenance of excitable membranes (e.g., during constant renewal of photoreceptor disc membranes). When radiolabeled 18:3n−3, the dietary precursor of 22:6n−3, is systemically supplied to 3-day-old mouse pups, it is elongated and desaturated in the liver, leading to the synthesis of 22:6n−3 – lipoproteins that shuttle the fatty acid through the bloodstream to retina and brain. When radiolabeled 22:6n−3 was used, a more efficient labeling of brain and retinal lipids was achieved. The retinal pigment epithelium is involved, not only in the uptake of 22:6n−3 from circulating lipoproteins in the choriocapillaris but also in the recycling of 22:6n−3 from degraded phagosomal phospholipids back to the inner segments of photoreceptors (the short loop), following each phagocytic event. An interplay among efficient 22:6n−6 delivery from the liver, selective uptake by retinal pigment epithelium photoreceptor cells, and avid retinal retention may contribute to the enrichment of excitable membranes of the retina with 22:6n−3 – phospholipids.Key words: docosahexaenoic acid, phospholipids, photoreceptors.

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