scholarly journals Expression of JAM-A in the Human Corneal Endothelium and Retinal Pigment Epithelium: Localization and Evidence for Role in Barrier Function

2007 ◽  
Vol 48 (9) ◽  
pp. 3928 ◽  
Author(s):  
Kenneth J. Mandell ◽  
Lennart Berglin ◽  
Eric A. Severson ◽  
Henry F. Edelhauser ◽  
Charles A. Parkos
Keyword(s):  
Retinal Pigment Epithelium ◽  
Barrier Function ◽  
Corneal Endothelium ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Human Corneal Endothelium

scholarly journals Pathogenic Effects of Mineralocorticoid Pathway Activation in Retinal Pigment Epithelium

2021 ◽  
Vol 22 (17) ◽  
pp. 9618
Author(s):  
Jérémie Canonica ◽  
Min Zhao ◽  
Tatiana Favez ◽  
Emmanuelle Gelizé ◽  
Laurent Jonet ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Retinal Pigment Epithelium ◽  
Barrier Function ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Retinal Diseases ◽  
Mesenchymal Transition ◽  
Rpe Cells ◽  
Pathway Activation ◽  
And Migration

Glucocorticoids are amongst the most used drugs to treat retinal diseases of various origins. Yet, the transcriptional regulations induced by glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) activation in retinal pigment epithelium cells (RPE) that form the outer blood–retina barrier are unknown. Levels of endogenous corticoids, ligands for MR and GR, were measured in human ocular media. Human RPE cells derived from induced pluripotent stem cells (iRPE) were used to analyze the pan-transcriptional regulations induced by aldosterone—an MR-specific agonist, or cortisol or cortisol + RU486—a GR antagonist. The retinal phenotype of transgenic mice that overexpress the human MR (P1.hMR) was analyzed. In the human eye, the main ligand for GR and MR is cortisol. The iRPE cells express functional GR and MR. The subset of genes regulated by aldosterone and by cortisol + RU-486, and not by cortisol alone, mimics an imbalance toward MR activation. They are involved in extracellular matrix remodeling (CNN1, MGP, AMTN), epithelial–mesenchymal transition, RPE cell proliferation and migration (ITGB3, PLAUR and FOSL1) and immune balance (TNFSF18 and PTX3). The P1.hMR mice showed choroidal vasodilation, focal alteration of the RPE/choroid interface and migration of RPE cells together with RPE barrier function alteration, similar to human retinal diseases within the pachychoroid spectrum. RPE is a corticosteroid-sensitive epithelium. MR pathway activation in the RPE regulates genes involved in barrier function, extracellular matrix, neural regulation and epithelial differentiation, which could contribute to retinal pathology.

scholarly journals Concerted regulation of retinal pigment epithelium basement membrane and barrier function by angiocrine factors

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Ignacio Benedicto ◽  
Guillermo L. Lehmann ◽  
Michael Ginsberg ◽  
Daniel J. Nolan ◽  
Rohan Bareja ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Basement Membrane ◽  
Barrier Function ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Angiocrine Factors

scholarly journals Grape Seed Proanthocyanindin Extract Moderated Retinal Pigment Epithelium Cellular Senescence Through NAMPT/SIRT1/NLRP3 Pathway

2021 ◽  
Author(s):  
Yan Wu ◽  
Sanyou Dai ◽  
Yang Long ◽  
Hongzhuo Liu ◽  
Weiwei Wan ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Cellular Senescence ◽  
Barrier Function ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Grape Seed ◽  
Rpe Cells ◽  
Mitochondrial Homeostasis

Abstract Background: Cellular senescence of retinal pigment epithelium (RPE) cell was an important cause of degenerative retinal disorders, however, the potential effects of grape seed proanthocyanindin extract (GSPE) through regulating NAMPT/SIRT1/NLRP3 pathway remained unclear.Methods: The effects of GSPE on the cellular senescence biomarkers as well as NAMPT and NAD+ contents were detected in both in-vivo and in-vitro RPE cell models. The protection of GSPE treatment on the mitochondrial homeostasis and barrier function of RPE cells were detected with mtDNA lesions, JC-1 staining, ZO1 expression, trans-epithelial cell resistance (TEER) as well as senescence-associated secretory phenotype (SASP) expressions. The GSPE treatment with NAMPT inhibitor, Fk866, and SIRT1 inhibitor, EX-527, was used in the potential NAMPT/SIRT1/NLRP3 mechanism detection.Results: GSPE significantly improve the NAMPT and NAD+ content in aging mice and thus alleviated the RPE cellular senescence. In advanced in-vitro studies, GSPE could be an activator of NAMPT and thus relieved H2O2 induced NAD+ depression. In advanced analyses, it was reported that GSPE could alleviate mitochondrial homeostasis, barrier function and SASP of aging RPE cells. Thus, detection the SASP in in-vitro aging model provided us knowledge in the understanding of the anti-aging role of GSPE and following detailed pathological mechanism analyses demonstrated that GSPE demonstrated the protective effects in aging RPE cells through NAMPT/SIRT1/NLRP3 pathway.Conclusions: These findings indicate that GSPE alleviated cellular senescence both in-vivo and in-vitro through NAMPT/SIRT1/NLRP3 pathway. This study highlighted the importance both the potential GSPE in degenerative retinopathy as well as the crosstalk of NAD+ metabolism, SIRT1 function and NLRP3 activation.

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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