scholarly journals Dopamine 2 Receptor Signaling Controls the Daily Burst in Phagocytic Activity in the Mouse Retinal Pigment Epithelium

2020 ◽  
Vol 61 (5) ◽  
pp. 10 ◽  
Author(s):  
Varunika Goyal ◽  
Christopher DeVera ◽  
Virginie Laurent ◽  
Jana Sellers ◽  
Micah A. Chrenek ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Phagocytic Activity ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Receptor Signaling ◽  
Dopamine 2 Receptor

scholarly journals Dopamine 2 receptor signaling controls the daily burst in phagocytic activity in the mouse retinal pigment epithelium

2019 ◽  
Author(s):  
Varunika Goyal ◽  
Christopher DeVera ◽  
Virginie Laurent ◽  
Jana Sellers ◽  
Micah A. Chrenek ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Pathway Analysis ◽  
Phagocytic Activity ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Early Morning ◽  
Integrin Signaling ◽  
One Year ◽  
Dopamine 2 Receptor ◽  
The Impact

AbstractPurposeA burst in phagocytosis of spent photoreceptor outer fragments by retinal pigment epithelium (RPE) is a rhythmic process occurring 1-2 hours after the onset of light. This phenomenon is considered crucial for the health of the photoreceptors and RPE. We have recently reported that dopamine, via dopamine 2 receptor (D2R), shifts the circadian rhythm in the RPE.MethodsHere, we first investigated the impact of the removal of D2R on the daily peak of phagocytosis by RPE and then we analyzed the function and morphology of retina and RPE in the absence of D2R.ResultsD2R KO mice do not show a daily burst of phagocytic activity after the onset of light. Also, in contrast to control, phosphorylation of FAK did not increase significantly in KO mice at ZT1. RNA sequencing revealed a total of 394 differentially expressed genes (DEGs) between ZT23 and ZT1 in the control mice, whereas in D2R KO mice, we detected 1054 DEGs. Pathway analysis of the gene expression data implicated integrin signaling to be one of the upregulated pathways in control but not in D2R KO mice. No difference in retinal thickness, visual function, or morphology of RPE cells was observed between WT and D2R KO mice at the age of 3 and 12 months.ConclusionsOur data suggest that removal of D2R prevents the burst in phagocytosis and a related increase in the phosphorylation of FAK after light onset. The pathway analysis points towards a putative role of D2R in controlling integrin signaling, which is known to play an important role in the control of the daily burst of phagocytosis by the RPE. Our data also indicate that the absence in the burst of phagocytic activity in the early morning does not produce any apparent deleterious effect on the retina or RPE up to one year of age.

scholarly journals Melatonin signaling affects the timing in the daily rhythm of phagocytic activity by the retinal pigment epithelium

2017 ◽  
Vol 165 ◽  
pp. 90-95 ◽  
Author(s):  
Virgine Laurent ◽  
Anamika Sengupta ◽  
Aída Sánchez-Bretaño ◽  
David Hicks ◽  
Gianluca Tosini
Keyword(s):  
Retinal Pigment Epithelium ◽  
Phagocytic Activity ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Daily Rhythm

scholarly journals THE CIRCADIAN CLOCK IN THE RETINAL PIGMENT EPITHELIUM CONTROLS THE DIURNAL RHYTHM OF PHAGOCYTIC ACTIVITY

2020 ◽  
Author(s):  
Christopher DeVera ◽  
Jendayi Dixon ◽  
Micah A. Chrenek ◽  
Kenkichi Baba ◽  
P. Michael Iuvone ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Circadian Clock ◽  
Phagocytic Activity ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Optomotor Response ◽  
Rpe Cells ◽  
Photoreceptor Outer Segments ◽  
Outer Segments ◽  
Old Mice

AbstractThe diurnal peak of phagocytosis by the retinal pigment epithelium (RPE) of photoreceptor outer segments (POS) is under circadian control, and it is believed that this process involves interactions from both the retina and RPE. Previous studies have demonstrated that a functional circadian clock exists within multiple retinal cell types and RPE cells. Thereby, the aim of the current study was to determine whether the circadian clock in the retina and or RPE controls the diurnal phagocytic peak of photoreceptor outer segments and whether selective disruption of the circadian clock in the RPE would affect RPE cells function and the viability during aging. To that aim, we first generated and validated an RPE tissue-specific KO of the essential clock gene, Bmal1, and then we determined the daily rhythm in phagocytic activity by the RPE in mice lacking a functional circadian clock in the retina or RPE. Then using electroretinography, spectral domain-optical coherence tomography, and optomotor response measurements of visual function we determined the effect of Bmal1 removal in young (6-month old) and old (18-month old) mice. RPE morphology and lipofuscin accumulation was also determined in young and old mice. Our data show that the circadian clock in the RPE controls the daily diurnal phagocytic peak of POS. Surprisingly, the lack of a functional RPE circadian clock or the diurnal phagocytic peak does not result in any detectable age-related degenerative phenotype in the retina or RPE. Thus, our results demonstrate that the loss of the circadian clock in the RPE or the lack of the daily peak in phagocytosis of POS does not result in deterioration of photoreceptors or the RPE during aging.

High-voltage electron microscopy of subretinal scar formation

1992 ◽  
Vol 50 (1) ◽  
pp. 486-487
Author(s):  
G.E. Korte ◽  
M. Marko ◽  
G. Hageman
Keyword(s):  
Electron Microscopy ◽  
Monoclonal Antibody ◽  
Retinal Pigment Epithelium ◽  
Glial Cells ◽  
High Voltage ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Sodium Iodate ◽  
High Voltage Electron Microscopy ◽  
Voltage Electron

Sodium iodate iv. damages the retinal pigment epithelium (RPE) in rabbits. Where RPE does not regenerate (e.g., 1,2) Muller glial cells (MC) forma subretinal scar that replaces RPE. The MC response was studied by HVEM in 3D computer reconstructions of serial thick sections, made using the STEREC0N program (3), and the HVEM at the NYS Dept. of Health in Albany, NY. Tissue was processed for HVEM or immunofluorescence localization of a monoclonal antibody recognizing MG microvilli (4).

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