Blue light effect on retinal pigment epithelial cells by display devices

2017 ◽  
Vol 9 (5) ◽  
pp. 436-443 ◽  
Author(s):  
Jiyoung Moon ◽  
Jieun Yun ◽  
Yeo Dae Yoon ◽  
Sang-Il Park ◽  
Young-Jun Seo ◽  
...  
Keyword(s):  
Blue Light ◽  
Retinal Pigment Epithelial ◽  
Retinal Pigment ◽  
Retinal Pigment Epithelial Cells ◽  
Light Effect ◽  
Rpe Cells ◽  
Display Devices ◽  
Low Intensity ◽  
Pigment Epithelial ◽  
Pigment Epithelial Cells

Even low-intensity blue light emitted by display devices exerts hazardous effects on RPE cells, which might be solved if display devices contain less short wavelength blue light.

Orientation of actin filaments in teleost retinal pigment epithelial cells, and the effect of the lectin, Concanavalin A, on melanosome motility

2014 ◽  
Vol 31 (1) ◽  
pp. 1-10 ◽  
Author(s):  
CHRISTINA KING-SMITH ◽  
RONALD J. VAGNOZZI ◽  
NICOLE E. FISCHER ◽  
PATRICK GANNON ◽  
SATYA GUNNAM
Keyword(s):  
Epithelial Cells ◽  
Actin Filament ◽  
Concanavalin A ◽  
Actin Filaments ◽  
Retinal Pigment Epithelial ◽  
Retinal Pigment ◽  
Retinal Pigment Epithelial Cells ◽  
Rpe Cells ◽  
Pigment Epithelial ◽  
Pigment Epithelial Cells

AbstractRetinal pigment epithelial cells of teleosts contain numerous melanosomes (pigment granules) that exhibit light-dependent motility. In light, melanosomes disperse out of the retinal pigment epithelium (RPE) cell body (CB) into long apical projections that interdigitate with rod photoreceptors, thus shielding the photoreceptors from bleaching. In darkness, melanosomes aggregate through the apical projections back into the CB. Previous research has demonstrated that melanosome motility in the RPE CB requires microtubules, but in the RPE apical projections, actin filaments are necessary and sufficient for motility. We used myosin S1 labeling and platinum replica shadowing of dissociated RPE cells to determine actin filament polarity in apical projections. Actin filament bundles within RPE apical projections are uniformly oriented with barbed ends toward the distal tips. Treatment of RPE cells with the tetravalent lectin, Concanavalin A, which has been shown to suppress cortical actin flow by crosslinking of cell-surface proteins, inhibited melanosome aggregation and stimulated ectopic filopodia formation but did not block melanosome dispersion. The polarity orientation of F-actin in apical projections suggests that a barbed-end directed myosin motor could effect dispersion of melanosomes from the CB into apical projections. Inhibition of aggregation, but not dispersion, by ConA confirms that different actin-dependent mechanisms control these two processes and suggests that melanosome aggregation is sensitive to treatments previously shown to disrupt actin cortical flow.

Carrier-dependent and carrier-independent uptake of myo-inositol in cultured retinal pigment epithelial cells: activation by heat and concentration

1988 ◽  
Vol 66 (9) ◽  
pp. 942-950 ◽  
Author(s):  
Mahin Khatami
Keyword(s):  
Retinal Pigment Epithelial ◽  
Retinal Pigment ◽  
Primary Cultures ◽  
Retinal Pigment Epithelial Cells ◽  
Transport Systems ◽  
Rate Equations ◽  
Rpe Cells ◽  
Major Mechanism ◽  
Pigment Epithelial ◽  
Pigment Epithelial Cells

Transport of myo-inositol (MI) was studied in primary cultures of bovine retinal pigment epithelial (RPE) cells. At low external concentrations (0.01–1 mM), uptake appeared to follow saturation kinetics, although the reciprocal forms of the rate equations did not fit either Lineweaver–Burk or Eadie–Hofstee plots. Increasing external concentrations dramatically changed the pattern of MI entry. At two to three orders of magnitude higher than physiological concentrations, a second saturation occurred (pseudo saturation). Cells incubated with 20 μM [3H]MI for 60 min had a ratio of intracellular to extracellular radioactivity ≥ 8, indicating active transport.MI transport reduction by Na+ replacement or inhibitors (phlorizin, ouabain, amiloride, KSCN, iodoacetamide, MI analogues) was greater when RPE cells were incubated with low (20–400 μM) than with high (10–20 mM) MI concentrations. Cells incubated with 20 μM MI at 53 or 65 °C showed increased transport (up to 560%) compared with cells at 22 °C. The effect on MI uptake (20 μM) of Na+ replacement also was reduced at 53 °C. The uptake of MI involved at least two transport systems. The major mechanism at low external MI concentrations (physiological levels) was a carrier-mediated active process. At high external MI levels, uptake occurred by a diffusion process. A lipotropic effect of MI may be responsible for this increased rate of diffusion.

scholarly journals Rat retinal pigment epithelial cells show specificity of phagocytosis in vitro.

1986 ◽  
Vol 103 (1) ◽  
pp. 299-308 ◽  
Author(s):  
P L Mayerson ◽  
M O Hall
Keyword(s):  
Cell Cultures ◽  
Retinal Pigment Epithelial ◽  
Retinal Pigment ◽  
Retinal Pigment Epithelial Cells ◽  
Rpe Cells ◽  
Pigment Epithelial ◽  
Retinal Rod ◽  
Immunofluorescence Labeling ◽  
Pigment Epithelial Cells

The retinal pigment epithelial (RPE) cell of the eye normally phagocytozes only retinal rod outer segments (ROS). The specificity of this phagocytic process was examined by incubating RPE cells with a variety of particle types. Confluent RPE cell cultures were incubated for 3 h at 37 degrees C in the presence of rat ROS, rat red blood cells (RBC), algae, bacteria, or yeast. Other cell cultures were incubated with equal numbers of ROS and one other particle type. Quantitative scanning electron microscopy was used to determine the numbers and morphology of particles bound to RPE cells, while double immunofluorescence labeling (Chaitin, M. H., and M. O. Hall, 1983, Invest. Ophthalmol. Vis. Sci., 24:812-820) was used to quantitate particle binding and ingestion. Both assays demonstrated phagocytosis to be a highly specific process. RPE cells bound 40-250 X more ROS than RBC, 30 X more ROS than algae, and 5 X more ROS than bacteria or yeast. Ingestion was more specific than binding; RPE cells ingested 970 X more ROS than RBC, 140 X more ROS than bacteria, and 35 X more ROS than yeast. The phagocytic preference for ROS was maintained in competition experiments with other particle types. Serum was found to be essential for phagocytosis. This study demonstrates that both the binding and ingestion phases of phagocytosis are highly specific processes.

scholarly journals PI3K/AKT/mTOR signaling participates in insulin‐mediated regulation of pathological myopia‐related factors in retinal pigment epithelial cells

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yunqin Li ◽  
Junliang Jiang ◽  
Jin Yang ◽  
Libo Xiao ◽  
Qiyun Hua ◽  
...  
Keyword(s):  
Retinal Pigment Epithelial ◽  
Insulin Treatment ◽  
Retinal Pigment ◽  
Mtor Signaling ◽  
Retinal Pigment Epithelial Cells ◽  
Pathological Myopia ◽  
Related Factors ◽  
Rpe Cells ◽  
Pigment Epithelial ◽  
Pigment Epithelial Cells

Abstract Background Insulin positively correlates with the length of the eye axis and is increased in the vitreous and serum of patients with pathological myopia (PM). How insulin influences the physiological process of retinal pigment epithelial (RPE) cells in PM remains unclear. This study aimed to explore the effect of insulin on the ultrastructure and function of RPE cells and the role of PI3K/AKT/mTOR signaling involved in the development of PM. Methods The ARPE-19 cells were treated with different concentrations of insulin to analyze the cell morphology, cell viability, the protein level of insulin receptor β, and the mRNA and protein levels of and PM-related factors (TIMP-2, MMP-2, bFGF, and IGF-1). The ultrastructure of APRE-19 cells was also observed after insulin treatment. Besides, the PI3K/AKT/mTOR signaling was studied with or without the PI3K inhibitor LY294002 in ARPE-19 cells. Results Insulin enhanced the cell viability of ARPE-19 cells and caused the endoplasmic reticulum to expand and vesiculate, suggesting increased secretion of growth factors and degeneration in ARPE-19 cells. Furthermore, the insulin receptor β was stimulated with insulin treatment, subsequently, the phosphorylation of AKT and mTOR was positively activated, which was adversely suppressed in the presence of LY294002. The secretion of TIMP-2 and bFGF was significantly decreased, and the secretion of MMP-2 and IGF-1 was highly elevated with insulin treatment depending on the concentration in ARPE-19 cells. Furthermore, the effect of insulin on PM-related proteins was restored with the addition of LY294002. Conclusions Our results indicated that insulin regulated the secretion of PM-related factors via the PI3K/AKT/mTOR signaling pathway in retinal pigment epithelial cells, and thus probably promoted the development of PM through transducing regulation signals from retina to choroid and sclera.

scholarly journals Neural retina-specific Aldh1a1 controls dorsal choroidal vascular development via Sox9 expression in retinal pigment epithelial cells

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
So Goto ◽  
Akishi Onishi ◽  
Kazuyo Misaki ◽  
Shigenobu Yonemura ◽  
Sunao Sugita ◽  
...  
Keyword(s):  
Retinal Pigment Epithelial ◽  
Retinal Pigment ◽  
Vascular Development ◽  
Neural Retina ◽  
Retinal Pigment Epithelial Cells ◽  
Deficient Diet ◽  
Rpe Cells ◽  
Retinoic Acids ◽  
Pigment Epithelial ◽  
Pigment Epithelial Cells

VEGF secreted from retinal pigment epithelial (RPE) cells is responsible for the choroidal vascular development; however, the molecular regulatory mechanism is unclear. We found that Aldh1a1–/– mice showed choroidal hypoplasia with insufficient vascularization in the dorsal region, although Aldh1a1, an enzyme that synthesizes retinoic acids (RAs), is expressed in the dorsal neural retina, not in the RPE/choroid complex. The level of VEGF in the RPE/choroid was significantly decreased in Aldh1a1–/– mice, and RA-dependent enhancement of VEGF was observed in primary RPE cells. An RA-deficient diet resulted in dorsal choroidal hypoplasia, and simple RA treatment of Aldh1a1–/– pregnant females suppressed choroid hypoplasia in their offspring. We also found downregulation of Sox9 in the dorsal neural retina and RPE of Aldh1a1–/– mice and RPE-specific disruption of Sox9 phenocopied Aldh1a1–/– choroidal development. These results suggest that RAs produced by Aldh1a1 in the neural retina directs dorsal choroidal vascular development via Sox9 upregulation in the dorsal RPE cells to enhance RPE-derived VEGF secretion.

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