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.

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 Role of Peoxisome Proliferator Activator Receptor on Blood Retinal Barrier Breakdown

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-4 ◽  
Author(s):  
Yasuo Yanagi
Keyword(s):  
Diabetic Retinopathy ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Critical Role ◽  
Blood Retinal Barrier ◽  
Early Diabetes ◽  
Pathological Conditions ◽  
Barrier Breakdown ◽  
Brb Breakdown

The retinal vessels have two barriers: the retinal pigment epithelium and the retinal vascular endothelium. Each barrier exhibits increased permeability under various pathological conditions. This condition is referred to as blood retinal barrier (BRB) breakdown. Clinically, the most frequently encountered condition causing BRB breakdown is diabetic retinopathy. In recent studies, inflammation has been linked to BRB breakdown and vascular leakage in diabetic retinopathy. Biological support for the role of inflammation in early diabetes is the adhesion of leukocytes to the retinal vasculature (leukostasis) observed in diabetic retinopathy. is a member of a ligand-activated nuclear receptor superfamily and plays a critical role in a variety of biological processes, including adipogenesis, glucose metabolism, angiogenesis, and inflammation. There is now strong experimental evidence to support the theory that inhibits diabetes-induced retinal leukostasis and leakage, playing an important role in the pathogenesis of diabetic retinopathy. Therapeutic targeting of may be beneficial to diabetic retinopathy.

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