scholarly journals Active ion transport pathways in the bovine retinal pigment epithelium.

1990 ◽  
Vol 424 (1) ◽  
pp. 283-300 ◽  
Author(s):  
S S Miller ◽  
J L Edelman
Keyword(s):  
Retinal Pigment Epithelium ◽  
Ion Transport ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Transport Pathways ◽  
Active Ion Transport

scholarly journals Cyclic AMP modulation of ion transport across frog retinal pigment epithelium. Measurements in the short-circuit state.

1984 ◽  
Vol 83 (6) ◽  
pp. 853-874 ◽  
Author(s):  
S Miller ◽  
D Farber
Keyword(s):  
Retinal Pigment Epithelium ◽  
Cyclic Amp ◽  
Ion Transport ◽  
Apical Membrane ◽  
Short Circuit ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Basolateral Membrane ◽  
Active Absorption ◽  
Apical Side

In the frog retinal pigment epithelium (RPE), the cellular levels of cyclic AMP (cAMP) were measured in control conditions and after treatment with substances that are known to inhibit phosphodiesterase (PDE) activity (isobutyl-1-methylxanthine, SQ65442) or stimulate adenylate cyclase activity (forskolin). The cAMP levels were elevated by a factor of 5-7 compared with the controls in PDE-treated tissues and by a factor of 18 in forskolin-treated tissues. The exogenous application of cAMP (1 mM), PDE inhibitors (0.5 mM), or forskolin (0.1 mM) all produced similar changes in epithelial electrical parameters, such as transepithelial potential (TEP) and resistance (Rt), as well as changes in active ion transport. Adding 1 mM cAMP to the solution bathing the apical membrane transiently increased the short-circuit current (SCC) and the TEP (apical side positive) and decreased Rt. Microelectrode experiments showed that the elevation in TEP is due mainly to a depolarization of the basal membrane followed by, and perhaps also accompanied by, a smaller hyperpolarization of the apical membrane. The ratio of the apical to the basolateral membrane resistance increased in the presence of cAMP, and this increase, coupled with the decrease in Rt and the basolateral membrane depolarization, is consistent with a conductance increase at the basolateral membrane. Radioactive tracer experiments showed that cAMP increased the active secretion of Na (choroid to retina) and the active absorption of K (retina to choroid). Cyclic AMP also abolished the active absorption of Cl across the RPE. In sum, elevated cellular levels of cAMP affect active and passive transport mechanisms at the apical and basolateral membranes of the bullfrog RPE.

scholarly journals Bestrophin Cl− channels are highly permeable to HCO3−

2008 ◽  
Vol 294 (6) ◽  
pp. C1371-C1377 ◽  
Author(s):  
Zhiqiang Qu ◽  
H. Criss Hartzell
Keyword(s):  
Retinal Pigment Epithelium ◽  
Ion Transport ◽  
Ph Regulation ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Reversal Potential ◽  
Hek Cells ◽  
Cl Channels

Bestrophin-1 (Best1) is a Cl− channel that is linked to various retinopathies in both humans and dogs. Dysfunction of the Best1 Cl− channel has been proposed to cause retinopathy because of altered Cl− transport across the retinal pigment epithelium (RPE). In addition to Cl−, many Cl− channels also transport HCO3−. Because HCO3− is physiologically important in pH regulation and in fluid and ion transport across the RPE, we measured the permeability and conductance of bestrophins to HCO3− relative to Cl−. Four human bestrophin homologs (hBest1, hBest2, hBest3, and hBest4) and mouse Best2 (mBest2) were expressed in HEK cells, and the relative HCO3− permeability ( PHCO3/ PCl) and conductance ( GHCO3/ GCl) were determined. PHCO3/ PCl was calculated from the change in reversal potential ( Erev) produced by replacing extracellular Cl− with HCO3−. hBest1 was highly permeable to HCO3− ( PHCO3/ PCl = ∼0.44). hBest2, hBest4, and mBest2 had an even higher relative HCO3− permeability ( PHCO3/ PCl = 0.6–0.7). All four bestrophins had HCO3− conductances that were nearly the same as Cl− ( GHCO3/ GCl = 0.9–1.1). Extracellular Na+ did not affect the permeation of hBest1 to HCO3−. At physiological HCO3− concentration, HCO3− was also highly conductive. The hBest1 disease-causing mutations Y85H, R92C, and W93C abolished both Cl− and HCO3− currents equally. The V78C mutation changed PHCO3/ PCl and GHCO3/ GCl of mBest2 channels. These results raise the possibility that disease-causing mutations in hBest1 produce disease by altering HCO3− homeostasis as well as Cl− transport in the retina.

scholarly journals Ion transport across the murine retinal pigment epithelium

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Sighvatur Saevar Arnason ◽  
Sunna Björg Skarphedinsdottir ◽  
Thor Eysteinsson
Keyword(s):  
Retinal Pigment Epithelium ◽  
Ion Transport ◽  
Pigment Epithelium ◽  
Retinal Pigment

scholarly journals Mechanisms of Ion Transport Across the Mouse Retinal Pigment Epithelium Measured In Vitro

2020 ◽  
Vol 61 (6) ◽  
pp. 31
Author(s):  
Sunna Bjorg Skarphedinsdottir ◽  
Thor Eysteinsson ◽  
Sighvatur Sævar Árnason
Keyword(s):  
Retinal Pigment Epithelium ◽  
Ion Transport ◽  
Pigment Epithelium ◽  
Retinal Pigment

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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