Expression and functional properties of unique inward rectifier K+ channel Kir7.1 in the porcine iris and retinal pigment epithelium

2003 ◽  
Vol 27 (5) ◽  
pp. 279-287 ◽  
Author(s):  
Kanako Yasuda ◽  
Masahiko Shimura ◽  
Toru Nakazawa ◽  
Hajime Sato ◽  
Hiroshi Tomita ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Functional Properties ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Inward Rectifier ◽  
K Channel

scholarly journals Ba2+ unmasks K+ modulation of the Na+-K+ pump in the frog retinal pigment epithelium.

1985 ◽  
Vol 86 (6) ◽  
pp. 853-876 ◽  
Author(s):  
E R Griff ◽  
Y Shirao ◽  
R H Steinberg
Keyword(s):  
Retinal Pigment Epithelium ◽  
Channel Blocker ◽  
Apical Membrane ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
K Channel ◽  
Evoked Responses ◽  
Physiological Conditions ◽  
Transepithelial Potential ◽  
Slow Piii

This paper presents electrophysiological evidence that small changes in [K+]o modulate the activity of the Na+-K+ pump on the apical membrane of the frog retinal pigment epithelium (RPE). This membrane also has a large relative K+ conductance so that lowering [K+]o hyperpolarizes it and therefore increases the transepithelial potential (TEP). Ba2+, a K+ channel blocker, eliminated these normal K+-evoked responses; in their place, lowering [K+]o evoked an apical depolarization and TEP decrease that were blocked by apical ouabain or strophanthidin. These data indicate that Ba2+ blocked the major K+ conductance(s) of the RPE apical membrane and unmasked a slowing of the normally hyperpolarizing electrogenic Na+-K+ pump caused by lowering [K+]o. Evidence is also presented that [K+]o modulates the pump in the isolated RPE under physiological conditions (i.e., without Ba2+). In the intact retina, light decreases subretinal [K+]o and produces the vitreal-positive c-wave of the electroretinogram (ERG) that originates primarily in the RPE from a hyperpolarization of the apical membrane and TEP increase. When Ba2+ was present in the retinal perfusate, the apical membrane depolarized in response to light and the TEP decreased so that the ERG c-wave inverted. The retinal component of the c-wave, slow PIII, was abolished by Ba2+. The effects of Ba2+ were completely reversible. We conclude that Ba2+ unmasks a slowing of the RPE Na+-K+ pump by the light-evoked decrease in [K+]o. Such a response would reduce the amplitude of the normal ERG c-wave.

scholarly journals Expression and polarized distribution of an inwardly rectifying K+channel, Kir4.1, in rat retinal pigment epithelium

1999 ◽  
Vol 520 (2) ◽  
pp. 373-381 ◽  
Author(s):  
Shunji Kusaka ◽  
Yoshiyuki Horio ◽  
Akikazu Fujita ◽  
Kenji Matsushita ◽  
Atsushi Inanobe ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
K Channel ◽  
Inwardly Rectifying

Volume regulation in cultured cells derived from human retinal pigment epithelium

1994 ◽  
Vol 266 (3) ◽  
pp. C676-C683 ◽  
Author(s):  
B. G. Kennedy
Keyword(s):  
Retinal Pigment Epithelium ◽  
Cultured Cells ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Regulatory Volume Decrease ◽  
K Channel ◽  
Volume Increase ◽  
Human Retinal Pigment Epithelium ◽  
Efflux Pathway ◽  
Volume Decrease

To characterize volume regulatory mechanisms, unidirectional Rb+ efflux and influx, unidirectional Cl- influx, and cell volume were measured in cultured human retinal pigment epithelium (HRPE). The HRPE was found to be capable of both regulatory volume increase (RVI), in response to a hypertonic challenge, and regulatory volume decrease (RVD), in response to a hypotonic challenge. Bumetanide-sensitive Rb+ influx increased almost threefold on incubation in a hypertonic (390 mosmol/kgH2O) medium. Bumetanide-insensitive Rb+ influx was activated by hypotonic (190 mosmol/kgH2O) challenge as well as by treatment with N-ethylmaleimide (NEM). Exposure to hypotonic media also activated unidirectional Cl- influx and unidirectional Rb+ efflux. Both the RVD and hypotonically activated Rb+ efflux were inhibited by the K(+)-channel blocker barium. On the other hand, hypotonically activated Rb+ influx was increased by barium treatment. In sum, the HRPE exhibits volume-sensitive transport mechanisms over a range of volumes from 190 to 390 mosmol/kgH2O. Cultured HRPE possess hypertonically activated Na-K-Cl cotransport, hypotonically activated K-Cl cotransport, and a barium-inhibitable hypotonically activated K+ efflux pathway.

scholarly journals Expression and permeation properties of the K + channel Kir7.1 in the retinal pigment epithelium

2001 ◽  
Vol 531 (2) ◽  
pp. 329-346 ◽  
Author(s):  
Masahiko Shimura ◽  
Yukun Yuan ◽  
Jinghua T. Chang ◽  
Suiyuan Zhang ◽  
Peter A. Campochiaro ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
K Channel ◽  
Permeation Properties

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).

scholarly journals 4-(Phenylsulfanyl) Butan-2-One Attenuates the Inflammatory Response Induced by Amyloid-β Oligomers in Retinal Pigment Epithelium Cells

Marine Drugs ◽  
2020 ◽  
Vol 19 (1) ◽  
pp. 1
Author(s):  
Peeraporn Varinthra ◽  
Shun-Ping Huang ◽  
Supin Chompoopong ◽  
Zhi-Hong Wen ◽  
Ingrid Y. Liu
Keyword(s):  
Retinal Pigment Epithelium ◽  
Inflammatory Response ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Amyloid Β ◽  
Age Related Macular Degeneration ◽  
Epithelial Cell Line ◽  
Age Related ◽  
Tnf Α ◽  
Cox 2

Age-related macular degeneration (AMD) is a progressive eye disease that causes irreversible impairment of central vision, and effective treatment is not yet available. Extracellular accumulation of amyloid-beta (Aβ) in drusen that lie under the retinal pigment epithelium (RPE) has been reported as one of the early signs of AMD and was found in more than 60% of Alzheimer’s disease (AD) patients. Extracellular deposition of Aβ can induce the expression of inflammatory cytokines such as IL-1β, TNF-α, COX-2, and iNOS in RPE cells. Thus, finding a compound that can effectively reduce the inflammatory response may help the treatment of AMD. In this research, we investigated the anti-inflammatory effect of the coral-derived compound 4-(phenylsulfanyl) butan-2-one (4-PSB-2) on Aβ1-42 oligomer (oAβ1-42) added to the human adult retinal pigment epithelial cell line (ARPE-19). Our results demonstrated that 4-PSB-2 can decrease the elevated expressions of TNF-α, COX-2, and iNOS via NF-κB signaling in ARPE-19 cells treated with oAβ1-42 without causing any cytotoxicity or notable side effects. This study suggests that 4-PSB-2 is a promising drug candidate for attenuation of AMD.

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