scholarly journals Stimulation of Retinal Pigment Epithelium With an α7 nAChR Agonist Leads to Müller Glia Dependent Neurogenesis in the Adult Mammalian Retina

2019 ◽  
Vol 60 (2) ◽  
pp. 570 ◽  
Author(s):  
Mark K. Webster ◽  
Betty J. Barnett ◽  
Megan L. Stanchfield ◽  
Joshua R. Paris ◽  
Sarah E. Webster ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Muller Glia ◽  
Müller Glia ◽  
Α7 Nachr ◽  
Mammalian Retina ◽  
Stimulation Of

scholarly journals Clinically visible progression indicators in age-related macular degeneration are transdifferentiated retinal pigment epithelium

2021 ◽  
Author(s):  
Dongfeng Cao ◽  
Belinda Leong ◽  
Jeffrey D. Messinger ◽  
Deepayan Kar ◽  
Thomas Ach ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Macular Degeneration ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Risk Indicators ◽  
Muller Glia ◽  
Müller Glia ◽  
Age Related ◽  
Oct Imaging

AbstractAge-related macular degeneration (AMD) is a common sight-threatening disease of older adults and treatment options are needed. Abnormalities of retinal pigment epithelium (RPE), supporting cells to photoreceptors and capillaries, are a hallmark. Clinical optical coherence tomography (OCT) imaging reveals hyperreflective foci (HRF) that confer risk for end-stage disease and are attributed to ectopic out-of-layer RPE. Using longitudinal OCT imaging of AMD patients, we demonstrate that the trajectory of one HRF form, RPE plume, parallels the retinal Henle fiber layer. Histology shows fully pigmented cells approaching and contacting retinal capillaries with RPE organelles dispersing along Müller glia columns. We used immunohistochemistry and a system of morphologic phenotypes to assess RPE functional repertoire in AMD. RPE corresponding to HRF loses immunoreactivity for retinoid processing proteins RPE65 and CRALBP, and gains immunoreactivity for immune cell markers CD68 and CD163. Müller glia retain CRALBP immunoreactivity. Gain- and loss-of-function for RPE starts with individual in-layer cells and extends to all abnormal phenotypes. Down-regulated RPE retinoid handling may contribute to slowed rod vision while Müller glia sustain cone vision. Ectopic RPE corresponding to HRF are emblematic of widespread transdifferentiation, motivating treatments targeting AMD pathology earlier than the initiation of atrophy. Data can propel new biomarkers and therapeutic strategies for AMD.One Sentence SummaryIn age-related macular degeneration retinal pigment epithelial cells transdifferentiate and migrate into the retina where they are clinically visible progression risk indicators.

Stimulation of inositol phosphate formation in cultured human retinal pigment epithelium

1992 ◽  
Vol 583 (1-2) ◽  
pp. 23-30 ◽  
Author(s):  
Richard B. Crook ◽  
Mi-Kyoung Song ◽  
Liliana P. Tong ◽  
Julie M. Yabu ◽  
Jon R. Polansky ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Inositol Phosphate ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Human Retinal Pigment Epithelium ◽  
Stimulation Of

scholarly journals Succinate can shuttle reducing power from the hypoxic retina to the O2-rich pigment epithelium

2020 ◽  
Author(s):  
Celia M. Bisbach ◽  
Daniel T. Hass ◽  
Brian M. Robbings ◽  
Austin M. Rountree ◽  
Martin Sadilek ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Succinate Dehydrogenase ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Reducing Power ◽  
Terminal Electron Acceptor ◽  
Transport Chain ◽  
Hypoxic Environment ◽  
Dehydrogenase Reaction ◽  
Mammalian Retina

AbstractWhen O2 is plentiful, the mitochondrial electron transport chain uses it as a terminal electron acceptor. However, the mammalian retina thrives within a hypoxic niche in the eye. We find that mitochondria in retinas adapt to their hypoxic environment by relying on the “reverse” succinate dehydrogenase reaction, where fumarate accepts electrons instead of O2. Reverse succinate dehydrogenase activity produces succinate and is enhanced by down-regulation of cytochrome oxidase subunits. Retinas can export the succinate to the neighboring retinal pigment epithelium/choroid complex. There, succinate stimulates O2 consumption several fold and enhances synthesis and release of malate. Malate released from the pigment epithelium can be imported into the retina, where it is converted to fumarate and again used to accept electrons in the reverse succinate dehydrogenase reaction. Our findings show how a malate/succinate shuttle can sustain these two tissues by transferring reducing power from an O2-poor tissue (retina) to an O2-rich one (retinal pigment epithelium/choroid).

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