The role of the retinal pigment epithelium and Müller cells secretome in neovascular retinal pathologies

Biochimie ◽  
2018 ◽  
Vol 155 ◽  
pp. 104-108 ◽  
Author(s):  
Rute S. Araújo ◽  
Daniela F. Santos ◽  
Gabriela A. Silva
Keyword(s):  
Retinal Pigment Epithelium ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Müller Cells ◽  
Muller Cells ◽  
Retinal Pathologies

scholarly journals Extracellular K+ activity changes related to electroretinogram components. II. Rabbit (E-type) retinas.

1985 ◽  
Vol 85 (6) ◽  
pp. 911-931 ◽  
Author(s):  
E Dick ◽  
R F Miller ◽  
S Bloomfield
Keyword(s):  
Retinal Pigment Epithelium ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Müller Cells ◽  
Extracellular Potassium ◽  
Muller Cells ◽  
Positive Component ◽  
Pharmacological Agents ◽  
Slow Piii ◽  
K Activity

Electroretinogram (ERG) and extracellular potassium activity (K+o) measurements were carried out in isolated superfused rabbit eyecup preparations under control conditions and during the application of pharmacological agents that selectively modify the light-responsive retinal network. Light-evoked K+o changes in the rabbit (E-type) retina resemble those previously described in amphibian (I-type) retinas. Different components of the light-evoked K+o changes can be distinguished on the bases of retinal depth, V vs. log I properties, and their responses to pharmacological agents. We find two separable sources of light-evoked increases in extracellular K+: a proximal source and a distal source. The properties of the distal light-evoked K+o increase are consistent with the hypothesis that it initiates a K+-mediated current through Müller cells that is detected as the primary voltage of the electroretinographic b-wave. These experiments also support previous studies indicating that both the corneal-positive component of c-wave and the corneal-negative slow PIII potential result from K+-mediated influences on, respectively, the retinal pigment epithelium and Müller cells.

scholarly journals Brimonidine Can Prevent In Vitro Hydroquinone Damage on Retinal Pigment Epithelium Cells and Retinal Müller Cells

2016 ◽  
Vol 32 (2) ◽  
pp. 102-108 ◽  
Author(s):  
Claudio Ramírez ◽  
Javier Cáceres-del-Carpio ◽  
Justin Chu ◽  
Joshua Chu ◽  
M. Tarek Moustafa ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Müller Cells ◽  
Muller Cells ◽  
Retinal Pigment Epithelium Cells ◽  
Epithelium Cells

scholarly journals Expression and Role of VEGF in the Adult Retinal Pigment Epithelium

2011 ◽  
Vol 52 (13) ◽  
pp. 9478 ◽  
Author(s):  
Knatokie M. Ford ◽  
Magali Saint-Geniez ◽  
Tony Walshe ◽  
Alisar Zahr ◽  
Patricia A. D'Amore
Keyword(s):  
Retinal Pigment Epithelium ◽  
Pigment Epithelium ◽  
Retinal Pigment

scholarly journals Mitochondrial Ceramide Effects on the Retinal Pigment Epithelium in Diabetes

2020 ◽  
Vol 21 (11) ◽  
pp. 3830 ◽  
Author(s):  
Yan Levitsky ◽  
Sandra S. Hammer ◽  
Kiera P. Fisher ◽  
Chao Huang ◽  
Travan L. Gentles ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Mitochondrial Function ◽  
High Glucose ◽  
Citrate Synthase ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Intercellular Adhesion Molecule ◽  
Early Event ◽  
Rpe Cells

Mitochondrial damage in the cells comprising inner (retinal endothelial cells) and outer (retinal pigment epithelium (RPE)) blood–retinal barriers (BRB) is known to precede the initial BRB breakdown and further histopathological abnormalities in diabetic retinopathy (DR). We previously demonstrated that activation of acid sphingomyelinase (ASM) is an important early event in the pathogenesis of DR, and recent studies have demonstrated that there is an intricate connection between ceramide and mitochondrial function. This study aimed to determine the role of ASM-dependent mitochondrial ceramide accumulation in diabetes-induced RPE cell damage. Mitochondria isolated from streptozotocin (STZ)-induced diabetic rat retinas (7 weeks duration) showed a 1.64 ± 0.29-fold increase in the ceramide-to-sphingomyelin ratio compared to controls. Conversely, the ceramide-to-sphingomyelin ratio was decreased in the mitochondria isolated from ASM-knockout mouse retinas compared to wild-type littermates, confirming the role of ASM in mitochondrial ceramide production. Cellular ceramide was elevated 2.67 ± 1.07-fold in RPE cells derived from diabetic donors compared to control donors, and these changes correlated with increased gene expression of IL-1β, IL-6, and ASM. Treatment of RPE cells derived from control donors with high glucose resulted in elevated ASM, vascular endothelial growth factor (VEGF), and intercellular adhesion molecule 1 (ICAM-1) mRNA. RPE from diabetic donors showed fragmented mitochondria and a 2.68 ± 0.66-fold decreased respiratory control ratio (RCR). Treatment of immortalized cell in vision research (ARPE-19) cells with high glucose resulted in a 25% ± 1.6% decrease in citrate synthase activity at 72 h. Inhibition of ASM with desipramine (15 μM, 1 h daily) abolished the decreases in metabolic functional parameters. Our results are consistent with diabetes-induced increase in mitochondrial ceramide through an ASM-dependent pathway leading to impaired mitochondrial function in the RPE cells of the retina.

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