scholarly journals Disruption of the blood-retinal barrier at the retinal pigment epithelium in hypertension

1992 ◽  
Vol 33 (4) ◽  
pp. 562-562
Author(s):  
Sigeki Takahasi ◽  
Izuru Asaoka ◽  
Hirosi Takamura ◽  
Takeo Satoh
Keyword(s):  
Retinal Pigment Epithelium ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Blood Retinal Barrier

Diffusible, retinal factors stimulate the barrier properties of junctional complexes in the retinal pigment epithelium

1993 ◽  
Vol 106 (3) ◽  
pp. 859-867 ◽  
Author(s):  
L.J. Rizzolo ◽  
Z.Q. Li
Keyword(s):  
Retinal Pigment Epithelium ◽  
Conditioned Medium ◽  
Tight Junctions ◽  
Electrical Resistance ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Neural Retina ◽  
Transepithelial Electrical Resistance ◽  
Blood Retinal Barrier ◽  
Junctional Complexes

The retinal pigment epithelium lies at the interface between the neural retina and the choriocapillaris where it forms a blood-retinal barrier. Barrier function requires a polarized distribution of plasma membrane proteins and ‘tight’ tight junctions. During chicken embryogenesis, these features develop gradually. Although terminal junctional complexes are established by embryonic day 4, the distribution of the Na+/K(+)-APTase is not polarized in all cells of the epithelium until embryonic day 11. Similarly, the tight junctions of early embryos are leaky, but become tight by hatching (embryonic day 21). We used primary cell culture to examine the molecular basis of this gradual induction of polarized function. Pigment epithelium harvested from embryonic day 7, and cultured on filters, formed monolayers coupled by junctional complexes. The distribution of the Na+/K(+)-ATPase was non-polarized and the tight junctions were leaky with a transepithelial electrical resistance of 20–30 omega cm2. To isolate diffusible factors that stimulate the transepithelial electrical resistance, neural retinas from embryonic day 7, 14 or 16 embryos were incubated at 37 degrees C in base medium for 6 hours. The conditioned medium was added to the apical chamber of freshly cultured pigment epithelium. The distribution of the Na+/K(+)-ATPase became basolateral, and the electrical resistance gradually increased two to three times over 6 days. The increase in electrical resistance corresponded to a decrease in the rate of [3H]inulin diffusion across the monolayer. The effectiveness of the conditioned medium increased steadily with increasing age of the neural retina. Rather than increased production of an active factor, apparently different active factors were produced at different ages.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Puerarin protects the retinal pigment epithelium (ARPE19) against hypoxia-induced blood-retinal barrier breakdown and Akt/Bcl2-dependent apoptosis

2021 ◽  
Author(s):  
Minh-Anh Nguyen Ngo Le ◽  
Yao-Tseng Wen ◽  
Dieu-Thuong Thi Trinh ◽  
Rong - Kung Tsai
Keyword(s):  
Retinal Pigment Epithelium ◽  
Group Treatment ◽  
Brain Injuries ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Annexin V ◽  
Blood Retinal Barrier ◽  
Hypoxic Conditions ◽  
Barrier Breakdown ◽  
Induced Apoptosis

Abstract Background: Puerarin, an isoflavonoid, is a neuroprotectant against many ischemic brain injuries. The research purpose was to investigate whether puerarin treatment can inhibit hypoxia-induced apoptosis and barrier breakdown on human retinal pigment epithelium (ARPE-19) cells.Methods: Treatment with 100 µM of puerarin showed no ARPE-19 cytotoxicity. Treatments with 50 µM or 100 µM of puerarin significantly preserved cell viability under hypoxic conditions for 12 h (p < 0.05). Moreover, treatments with 50 µM and 100 µM of puerarin significantly reduced the proportion of Annexin V- and PI-positive ARPE cells under hypoxic conditions (p < 0.05). The TER analysis and junctional protein staining demonstrated that treatments with 50 µM or 100 µM of puerarin prevented the hypoxia-induced barrier disruption in APRE-19 cultures. In contrast to the untreated group, treatment with puerarin significantly increased the level of Bcl-2 and decreased the levels of p-Bad, Bax, and cleaved caspase 3 in RPE cell under hypoxic conditions (p < 0.05). Treatment with puerarin maintained Akt1 activation in the ARPE-19 cells under hypoxic conditions (p < 0.05), and inhibition of PR-induced Akt1 activation abolished the protective effect of puerarin in ARPE-19 cells under hypoxic conditions.Conclusion: Our results demonstrated that treatment with puerarin protected RPE cell against hypoxia-induced blood-retinal barrier breakdown and Akt-dependent apoptosis. These findings suggest that puerarin could be developed as an alternative treatment for ischemic and hypoxic retinal injuries.

DISRUPTION OF BLOOD-RETINAL BARRIER AT THE RETINAL PIGMENT EPITHELIUM AFTER SYSTEMIC UREA INJECTION

2009 ◽  
Vol 56 (1) ◽  
pp. 27-39 ◽  
Author(s):  
SATOSHI OKINAMI ◽  
MASATO OHKUMA ◽  
MINORU OHTA ◽  
ISAMU TSUKAHARA
Keyword(s):  
Retinal Pigment Epithelium ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Blood Retinal Barrier

scholarly journals The Retinal Pigment Epithelium: Something More than a Constituent of the Blood-Retinal Barrier—Implications for the Pathogenesis of Diabetic Retinopathy

2010 ◽  
Vol 2010 ◽  
pp. 1-15 ◽  
Author(s):  
Rafael Simó ◽  
Marta Villarroel ◽  
Lídia Corraliza ◽  
Cristina Hernández ◽  
Marta Garcia-Ramírez
Keyword(s):  
Diabetic Retinopathy ◽  
Retinal Pigment Epithelium ◽  
Structural Integrity ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Secretory Activity ◽  
Therapeutic Strategies ◽  
Blood Retinal Barrier ◽  
Absorption Of Light ◽  
Photoreceptor Membranes

The retinal pigment epithelium (RPE) is an specialized epithelium lying in the interface between the neural retina and the choriocapillaris where it forms the outer blood-retinal barrier (BRB). The main functions of the RPE are the following: (1) transport of nutrients, ions, and water, (2) absorption of light and protection against photooxidation, (3) reisomerization of all-trans-retinal into 11-cis-retinal, which is crucial for the visual cycle, (4) phagocytosis of shed photoreceptor membranes, and (5) secretion of essential factors for the structural integrity of the retina. An overview of these functions will be given. Most of the research on the physiopathology of diabetic retinopathy has been focused on the impairment of the neuroretina and the breakdown of the inner BRB. By contrast, the effects of diabetes on the RPE and in particular on its secretory activity have received less attention. In this regard, new therapeutic strategies addressed to modulating RPE impairment are warranted.

scholarly journals Retinal Pigment Epithelium Remodeling in Mouse Models of Retinitis Pigmentosa

2021 ◽  
Vol 22 (10) ◽  
pp. 5381
Author(s):  
Debora Napoli ◽  
Martina Biagioni ◽  
Federico Billeri ◽  
Beatrice Di Marco ◽  
Noemi Orsini ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Retinitis Pigmentosa ◽  
Structural Integrity ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Barrier Dysfunction ◽  
Blood Retinal Barrier ◽  
Quantitative Image ◽  
Fluorescent Dextran

In retinitis pigmentosa (RP), one of many possible genetic mutations causes rod degeneration, followed by cone secondary death leading to blindness. Accumulating evidence indicates that rod death triggers multiple, non-cell-autonomous processes, which include oxidative stress and inflammation/immune responses, all contributing to cone demise. Inflammation relies on local microglia and recruitment of immune cells, reaching the retina through breakdowns of the inner blood retinal barrier (iBRB). Leakage in the inner retina vasculature suggests similarly altered outer BRB, formed by junctions between retinal pigment epithelium (RPE) cells, which are crucial for retinal homeostasis, immune response, and privilege. We investigated the RPE structural integrity in three models of RP (rd9, rd10, and Tvrm4 mice) by immunostaining for zonula occludens-1 (ZO-1), an essential regulatory component of tight junctions. Quantitative image analysis demonstrated discontinuities in ZO-1 profiles in all mutants, despite different degrees of photoreceptor loss. ZO-1 interruption zones corresponded to leakage of in vivo administered, fluorescent dextran through the choroid-RPE interface, demonstrating barrier dysfunction. Dexamethasone, administered to rd10 mice for rescuing cones, also rescued RPE structure. Thus, previously undetected, stereotyped abnormalities occur in the RPE of RP mice; pharmacological targeting of inflammation supports a feedback loop leading to simultaneous protection of cones and the RPE.

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