Intrachoroidal Dye Leakage in Indocyanine Green Fundus Angiography after Experimental Commotio Retinae

1992 ◽  
Vol 2 (2) ◽  
pp. 79-82 ◽  
Author(s):  
T. Miki ◽  
K. Kitashoji ◽  
T. Kohno
Keyword(s):  
Indocyanine Green ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Molecular Size ◽  
Sodium Fluorescein ◽  
Blood Retinal Barrier ◽  
Rabbit Eye ◽  
Icg Angiography ◽  
Commotio Retinae ◽  
Choroidal Vessels

Dye leakage in sodium fluorescein (FLUO) fundus angiography indicates damage to the blood-retinal barrier. However, dye leakage in indocyanine green (ICG) fundus angiography does not mean the same, because of the larger molecular size of the dye and impermeability of the choroidal vessels to it. The possibility of dye leakage in ICG angiography has not yet been revealed in an experimental study in which the blood-retinal barrier is undamaged. We report here that intrachoroidal dye leakage may occur in ICG angiography in an experimental model of the traumatic retinal opacity of the rabbit eye, even when the blood-retinal barrier is undamaged. This mechanism of dye leakage in ICG angiography is quite different from the leakage of FLUO angiography. Pathological choroidal vessels with increased permeability, such as choroidal neovascularization under the retinal pigment epithelium, can be observed using ICG angiography.

scholarly journals The Impact of Oxidative Stress on Blood-Retinal Barrier Physiology in Age-Related Macular Degeneration

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 64
Author(s):  
Annamaria Tisi ◽  
Marco Feligioni ◽  
Maurizio Passacantando ◽  
Marco Ciancaglini ◽  
Rita Maccarone
Keyword(s):  
Oxidative Stress ◽  
Macular Degeneration ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Blood Retinal Barrier ◽  
Functional Changes ◽  
Beneficial Effects ◽  
Age Related ◽  
The Impact

The blood retinal barrier (BRB) is a fundamental eye component, whose function is to select the flow of molecules from the blood to the retina and vice-versa, and its integrity allows the maintenance of a finely regulated microenvironment. The outer BRB, composed by the choriocapillaris, the Bruch’s membrane, and the retinal pigment epithelium, undergoes structural and functional changes in age-related macular degeneration (AMD), the leading cause of blindness worldwide. BRB alterations lead to retinal dysfunction and neurodegeneration. Several risk factors have been associated with AMD onset in the past decades and oxidative stress is widely recognized as a key factor, even if the exact AMD pathophysiology has not been exactly elucidated yet. The present review describes the BRB physiology, the BRB changes occurring in AMD, the role of oxidative stress in AMD with a focus on the outer BRB structures. Moreover, we propose the use of cerium oxide nanoparticles as a new powerful anti-oxidant agent to combat AMD, based on the relevant existing data which demonstrated their beneficial effects in protecting the outer BRB in animal models of AMD.

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

scholarly journals C-reactive protein isoforms differentially affect outer blood-retinal barrier integrity and function

2017 ◽  
Vol 312 (3) ◽  
pp. C244-C253 ◽  
Author(s):  
Blanca Molins ◽  
Anna Pascual ◽  
Méndez ◽  
Victor Llorenç ◽  
Javier Zarranz-Ventura ◽  
...  
Keyword(s):  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Protein Isoforms ◽  
Age Related Macular Degeneration ◽  
C Reactive Protein ◽  
Barrier Dysfunction ◽  
Blood Retinal Barrier ◽  
Reactive Protein ◽  
Anti Vegf ◽  
Age Related

The retinal pigment epithelium (RPE) forms the outer blood-retinal barrier (oBRB) and is the prime target of early age-related macular degeneration (AMD). C-reactive protein (CRP), a serum biomarker for chronic inflammation and AMD, presents two different isoforms, monomeric (mCRP) and pentameric (pCRP), that may have a different effect on inflammation and barrier function in the RPE. The results reported in this study suggest that mCRP but not pCRP impairs RPE functionality by increasing paracellular permeability and disrupting the tight junction proteins ZO-1 and occludin in RPE cells. Additionally, we evaluated the effect of drugs commonly used in clinical settings on mCRP-induced barrier dysfunction. We found that a corticosteroid (methylprednisolone) and an anti-VEGF agent (bevacizumab) prevented mCRP-induced ARPE-19 barrier disruption and IL-8 production. Furthermore, bevacizumab was also able to revert mCRP-induced IL-8 increase after mCRP stimulation. In conclusion, the presence of mCRP within retinal tissue may lead to disruption of the oBRB, an effect that may be modified in the presence of corticosteroids or anti-VEGF drugs.

scholarly journals Oxidative stress-mediated TXNIP loss causes RPE dysfunction

2019 ◽  
Vol 51 (10) ◽  
pp. 1-13 ◽  
Author(s):  
Min Ji Cho ◽  
Sung-Jin Yoon ◽  
Wooil Kim ◽  
Jongjin Park ◽  
Jangwook Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Function ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Common Factor ◽  
Age Related Macular Degeneration ◽  
Autophagic Flux ◽  
Blood Retinal Barrier ◽  
Rpe Cells ◽  
Age Related

Abstract The disruption of the retinal pigment epithelium (RPE), for example, through oxidative damage, is a common factor underlying age-related macular degeneration (AMD). Aberrant autophagy also contributes to AMD pathology, as autophagy maintains RPE homeostasis to ensure blood–retinal barrier (BRB) integrity and protect photoreceptors. Thioredoxin-interacting protein (TXNIP) promotes cellular oxidative stress by inhibiting thioredoxin reducing capacity and is in turn inversely regulated by reactive oxygen species levels; however, its role in oxidative stress-induced RPE cell dysfunction and the mechanistic link between TXNIP and autophagy are largely unknown. Here, we observed that TXNIP expression was rapidly downregulated in RPE cells under oxidative stress and that RPE cell proliferation was decreased. TXNIP knockdown demonstrated that the suppression of proliferation resulted from TXNIP depletion-induced autophagic flux, causing increased p53 activation via nuclear localization, which in turn enhanced AMPK phosphorylation and activation. Moreover, TXNIP downregulation further negatively impacted BRB integrity by disrupting RPE cell tight junctions and enhancing cell motility by phosphorylating, and thereby activating, Src kinase. Finally, we also revealed that TXNIP knockdown upregulated HIF-1α, leading to the enhanced secretion of VEGF from RPE cells and the stimulation of angiogenesis in cocultured human retinal microvascular endothelial cells. This suggests that the exposure of RPE cells to sustained oxidative stress may promote choroidal neovascularization, another AMD pathology. Together, these findings reveal three distinct mechanisms by which TXNIP downregulation disrupts RPE cell function and thereby exacerbates AMD pathogenesis. Accordingly, reinforcing or restoring BRB integrity by targeting TXNIP may serve as an effective therapeutic strategy for preventing or attenuating photoreceptor damage in AMD.

scholarly journals IFNγ regulates retinal pigment epithelial fluid transport

2009 ◽  
Vol 297 (6) ◽  
pp. C1452-C1465 ◽  
Author(s):  
Rong Li ◽  
Arvydas Maminishkis ◽  
Tina Banzon ◽  
Qin Wan ◽  
Stephen Jalickee ◽  
...  
Keyword(s):  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Basolateral Membrane ◽  
Primary Cultures ◽  
Mapk Signaling ◽  
Therapeutic Interventions ◽  
Subretinal Space ◽  
Fluid Absorption ◽  
Blood Retinal Barrier

The present experiments show that IFNγ receptors are mainly localized to the basolateral membrane of human retinal pigment epithelium (RPE). Activation of these receptors in primary cultures of human fetal RPE inhibited cell proliferation and migration, decreased RPE mitochondrial membrane potential, altered transepithelial potential and resistance, and significantly increased transepithelial fluid absorption. These effects are mediated through JAK-STAT and p38 MAPK signaling pathways. Second messenger signaling through cAMP-PKA pathway- and interferon regulatory factor-1-dependent production of nitric oxide/cGMP stimulated the CFTR at the basolateral membrane and increased transepithelial fluid absorption. In vivo experiments using a rat model of retinal reattachment showed that IFNγ applied to the anterior surface of the eye can remove extra fluid deposited in the extracellular or subretinal space between the retinal photoreceptors and RPE. Removal of this extra fluid was blocked by a combination of PKA and JAK-STAT pathway inhibitors injected into the subretinal space. These results demonstrate a protective role for IFNγ in regulating retinal hydration across the outer blood-retinal barrier in inflammatory disease processes and provide the basis for possible therapeutic interventions.

Effect ofToxoplasma gondiiinfection on the junctional complex of retinal pigment epithelial cells

Parasitology ◽  
2016 ◽  
Vol 143 (5) ◽  
pp. 568-575 ◽  
Author(s):  
ALANDERSON R. NOGUEIRA ◽  
FERNANDA LEVE ◽  
JOSÉ MORGADO-DIAZ ◽  
ROBERTO CARLOS TEDESCO ◽  
MIRIAN CLAUDIA S. PEREIRA
Keyword(s):  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Retinal Pigment Epithelial Cells ◽  
Ocular Toxoplasmosis ◽  
Junctional Complex ◽  
Cell Contact ◽  
Barrier Dysfunction ◽  
Blood Retinal Barrier ◽  
Retinal Injury ◽  
Transmission Electron

SUMMARYOcular toxoplasmosis is the most frequent cause of uveitis, leading to partial or total loss of vision, with the retina the main affected structure. The cells of the retinal pigment epithelium (RPE) play an important role in the physiology of the retina and formation of the blood–retinal barrier. Several pathogens induce barrier dysfunction by altering tight junction (TJ) integrity. Here, we analysed the effect of infection byToxoplasma gondiion TJ integrity in ARPE-19 cells. Loss of TJ integrity was demonstrated inT. gondii-infected ARPE-19 cells, causing increase in paracellular permeability and disturbance of the barrier function of the RPE. Confocal microscopy also revealed alteration in the TJ protein occludin induced byT. gondiiinfection. Disruption of junctional complex was also evidenced by scanning and transmission electron microscopy. Cell–cell contact loss was noticed in the early stages of infection byT. gondiiwith the visualization of small to moderate intercellular spaces. Large gaps were mostly observed with the progression of the infection. Thus, our data suggest that the alterations induced byT. gondiiin the structural organization of the RPE may contribute to retinal injury evidenced by ocular toxoplasmosis.

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