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Journal articles on the topic 'Blood retinal barrier'

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Author: Grafiati

Published: 4 June 2021

Last updated: 11 March 2023

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1

Yemanyi, Felix, Kiran Bora, Alexandra K. Blomfield, Zhongxiao Wang, and Jing Chen. "Wnt Signaling in Inner Blood–Retinal Barrier Maintenance." International Journal of Molecular Sciences 22, no. 21 (November 2, 2021): 11877. http://dx.doi.org/10.3390/ijms222111877.

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The retina is a light-sensing ocular tissue that sends information to the brain to enable vision. The blood–retinal barrier (BRB) contributes to maintaining homeostasis in the retinal microenvironment by selectively regulating flux of molecules between systemic circulation and the retina. Maintaining such physiological balance is fundamental to visual function by facilitating the delivery of nutrients and oxygen and for protection from blood-borne toxins. The inner BRB (iBRB), composed mostly of inner retinal vasculature, controls substance exchange mainly via transportation processes between (paracellular) and through (transcellular) the retinal microvascular endothelium. Disruption of iBRB, characterized by retinal edema, is observed in many eye diseases and disturbs the physiological quiescence in the retina’s extracellular space, resulting in vision loss. Consequently, understanding the mechanisms of iBRB formation, maintenance, and breakdown is pivotal to discovering potential targets to restore function to compromised physiological barriers. These unraveled targets can also inform potential drug delivery strategies across the BRB and the blood–brain barrier into retinas and brain tissues, respectively. This review summarizes mechanistic insights into the development and maintenance of iBRB in health and disease, with a specific focus on the Wnt signaling pathway and its regulatory role in both paracellular and transcellular transport across the retinal vascular endothelium.

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2

Cunha-Vaz, José. "The Blood–Retinal Barrier in Retinal Disease." European Ophthalmic Review 03, no. 02 (2009): 105. http://dx.doi.org/10.17925/eor.2009.03.02.105.

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The blood–ocular barrier system is formed by two main barriers: the blood–aqueous barrier and the blood–retinal barrier (BRB). The BRB is particularly tight and restrictive and is a physiological barrier that regulates ion, protein and water flux into and out of the retina. The BRB consists of inner and outer components, the inner BRB being formed of tight junctions between retinal capillary endothelial cells and the outer BRB of tight junctions between retinal pigment epithelial cells. The BRB is essential to maintaining the eye as a privileged site and is essential for normal visual function. Alterations of the BRB play a crucial role in the development of retinal diseases. The two most frequent and relevant retinal diseases, diabetic retinopathy and age-related macular degeneration (AMD), are directly associated with alterations of the BRB. Diabetic retinopathy is initiated by an alteration of the inner BRB and neovascular AMD is a result of an alteration of the outer BRB. Treatment of retinal diseases must also deal with the BRB either by using its specific transport mechanisms or by circumventing it through intravitreal injections

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3

Cunha-Vaz, José, Rui Bernardes, and Conceição Lobo. "Blood-Retinal Barrier." European Journal of Ophthalmology 21, no. 6_suppl (November 2011): 3–9. http://dx.doi.org/10.5301/ejo.2010.6049.

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4

Vinores, S. A., R. McGehee, A. Lee, C. Gadegbeku, and P. A. Campochiaro. "Ultrastructural localization of blood-retinal barrier breakdown in diabetic and galactosemic rats." Journal of Histochemistry & Cytochemistry 38, no. 9 (September 1990): 1341–52. http://dx.doi.org/10.1177/38.9.2117624.

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Breakdown of the blood-retinal barrier (BRB) is an early event in diabetic and galactosemic rats, but the location and nature of the specific defect(s) are controversial. Using an electron microscopic immunocytochemical technique, the retinas of normal, diabetic, and galactosemic rats were immunostained for endogenous albumin. Normal rats showed little evidence of BRB breakdown at either the inner barrier (retinal vasculature) or the outer barrier (retinal pigment epithelium) (RPE). In diabetic and galactosemic rats, as was true in human diabetics, BRB breakdown occurred predominantly at the inner BRB, but in some cases at the outer barrier as well. Treatment with the aldose reductase inhibitor sorbinil largely prevented BRB failure in galactosemic rats. In the inner retina of diabetic and galactosemic rats, albumin was frequently demonstrated on the abluminal side of the retinal capillary endothelium (RCE) in intercellular spaces, basal laminae, pericytes, ganglion cells, astrocytes, and the perinuclear cytoplasm of cells in the inner nuclear layer. Albumin did not appear to cross RCE cell junctions; however, it was occasionally seen in RCE cytoplasm of galactosemic rats. In the outer retina, albumin was frequently detected in the subretinal space, in the intercellular space between photoreceptors, and in the perinuclear cytoplasm of photoreceptor cells, but was only infrequently found in the RPE cells constituting the barrier. Albumin derived from the choroidal vasculature did not appear to cross the tight junctions of the RPE. These findings suggest that specific sites of BRB compromise are infrequent but that once albumin has crossed the RCE or RPE it freely permeates the retinal tissue by filling intercellular spaces and permeating the membranes of cells not implicated in BRB formation. The diffuse cytoplasmic staining of some RCE and RPE cells suggests that the predominant means of BRB breakdown in diabetes and galactosemia involves increased focal permeability of the surface membranes of the RCE and RPE cells rather than defective tight junctions or vesicular transport.

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5

Naylor, Aisling, Alan Hopkins, Natalie Hudson, and Matthew Campbell. "Tight Junctions of the Outer Blood Retina Barrier." International Journal of Molecular Sciences 21, no. 1 (December 27, 2019): 211. http://dx.doi.org/10.3390/ijms21010211.

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The outer blood retina barrier (oBRB) formed by the retinal pigment epithelium (RPE) is critical for maintaining retinal homeostasis. Critical to this modified neuro-epithelial barrier is the presence of the tight junction structure that is formed at the apical periphery of contacting cells. This tight junction complex mediates size-selective passive diffusion of solutes to and from the outer segments of the retina. Unlike other epithelial cells, the apical surface of the RPE is in direct contact with neural tissue and it is centrally involved in the daily phagocytosis of the effete tips of photoreceptor cells. While much is known about the intracellular trafficking of material within the RPE, less is known about the role of the tight junction complexes in health and diseased states. Here, we provide a succinct overview of the molecular composition of the RPE tight junction complex in addition to highlighting some of the most common retinopathies that involve a dysregulation of RPE integrity

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6

MENDES-JORGE, L., D. RAMOS, M. LUPPO, A. VALENçA, J. CATITA, CM DUARTE, M. SIMõES, et al. "Blood-retinal barrier serum ferritin transport in mouse retina." Acta Ophthalmologica 90 (August 6, 2012): 0. http://dx.doi.org/10.1111/j.1755-3768.2012.t029.x.

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7

Silva, Rufino M., J. R. Faria de Abreu, and J. G. Cunha-Vaz. "Blood-retina barrier in acute retinal branch vein occlusion." Graefe's Archive for Clinical and Experimental Ophthalmology 233, no. 11 (November 1995): 721–26. http://dx.doi.org/10.1007/bf00164677.

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8

Yanagi, Yasuo. "Role of Peoxisome Proliferator Activator Receptor on Blood Retinal Barrier Breakdown." PPAR Research 2008 (2008): 1–4. http://dx.doi.org/10.1155/2008/679237.

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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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9

Kubo, Yoshiyuki, Shinichi Akanuma, and Ken-ichi Hosoya. "The blood-retinal barrier transporters in retinal drug delivery." Drug Delivery System 27, no. 5 (2012): 361–69. http://dx.doi.org/10.2745/dds.27.361.

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10

D, Shah. "Resolution of Bilateral Exudative Retinal Detachment Secondary to Renal Hypertension with Systemic Management." Open Access Journal of Ophthalmology 7, no. 2 (July 1, 2022): 1–2. http://dx.doi.org/10.23880/oajo-16000252.

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Exudative retinal detachment (ERD) is an ocular condition, which develops from pathological conditions that disrupt the integrity of blood-retinal barrier due to fluid accumulation in sub retinal space or under neurosensory retina. Exudative retinal detachment is typically associated with inflammatory, infectious, neoplastic, and vascular pathological conditions. We report the management of bilateral exudative retinal detachment in young patients secondary to Renal Hypertension.

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11

Hosoya, Ken-ichi, Shin-ichi Akanuma, and Yoshiyuki Kubo. "Role of the Blood-Retinal Barrier Transporters: Antiaging in Retina." YAKUGAKU ZASSHI 141, no. 12 (December 1, 2021): 1319–25. http://dx.doi.org/10.1248/yakushi.21-00158-2.

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12

Acharya, Nimish K., Xin Qi, Eric L. Goldwaser, George A. Godsey, Hao Wu, Mary C. Kosciuk, Theresa A. Freeman, et al. "Retinal pathology is associated with increased blood–retina barrier permeability in a diabetic and hypercholesterolaemic pig model: Beneficial effects of the LpPLA2 inhibitor Darapladib." Diabetes and Vascular Disease Research 14, no. 3 (March 1, 2017): 200–213. http://dx.doi.org/10.1177/1479164116683149.

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Using a porcine model of diabetes mellitus and hypercholesterolaemia, we previously showed that diabetes mellitus and hypercholesterolaemia is associated with a chronic increase in blood–brain barrier permeability in the cerebral cortex, leading to selective binding of immunoglobulin G and deposition of amyloid-beta1-42 peptide in pyramidal neurons. Treatment with Darapladib (GlaxoSmithKline, SB480848), an inhibitor of lipoprotein-associated phospholipase-A2, alleviated these effects. Here, investigation of the effects of chronic diabetes mellitus and hypercholesterolaemia on the pig retina revealed a corresponding increased permeability of the blood–retina barrier coupled with a leak of plasma components into the retina, alterations in retinal architecture, selective IgG binding to neurons in the ganglion cell layer, thinning of retinal layers due to cell loss and increased glial fibrillary acidic protein expression in Müller cells, all of which were curtailed by treatment with Darapladib. These findings suggest that chronic diabetes mellitus and hypercholesterolaemia induces increased blood–retina barrier permeability that may be linked to altered expression of blood–retina barrier–associated tight junction proteins, claudin and occludin, leading to structural changes in the retina consistent with diabetic retinopathy. Additionally, results suggest that drugs with vascular anti-inflammatory properties, such as Darapladib, may have beneficial effects on eye diseases strongly linked to vascular abnormalities such as diabetic retinopathy and age-related macular degeneration.

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13

Toda, Ryotaro, Kouichi Kawazu, Masanobu Oyabu, Tatsuya Miyazaki, and Yoshiaki Kiuchi. "Comparison of Drug Permeabilities Across the Blood–Retinal Barrier, Blood–Aqueous Humor Barrier, and Blood–Brain Barrier." Journal of Pharmaceutical Sciences 100, no. 9 (September 2011): 3904–11. http://dx.doi.org/10.1002/jps.22610.

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14

Bernardes,, Rui, Pedro Serranho, Torcato Santos, Valter Gonçalves, and José Cunha Vaz. "Optical Coherence Tomography ? Automatic Retina Classification Through Support Vector Machines." European Ophthalmic Review 06, no. 04 (2012): 200. http://dx.doi.org/10.17925/eor.2012.06.04.200.

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Optical coherence tomography (OCT) is becoming one of the most important imaging modalities in ophthalmology due to its non-invasiveness and by allowing the visualisation the human retina structure in detail. It was recently proposed that OCT data embeds functional information from the human retina. Specifically, it was proposed that blood-retinal barrier status information is present within OCT data from the human retina. Besides this ability, the authors present data supporting the idea of having the OCT data encoding the ageing of the retina in addition to the disease (diabetes) condition from the healthy status. The methodology followed makes use of a supervised classification procedure, the support vector machine (SVM) classifier – based solely on the statistics of the distribution of OCT data from the human retina (i.e. OCT data between the inner limiting membrane and the retinal pigment epithelium). Results achieved suggest that information on both the healthy status of the blood–retinal barrier and on the ageing process co-exist encoded within the optical properties of the human retina.

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15

Wang, Zhongxiao, Chi-Hsiu Liu, Shuo Huang, Zhongjie Fu, Yohei Tomita, William R. Britton, Steve S. Cho, et al. "Wnt signaling activates MFSD2A to suppress vascular endothelial transcytosis and maintain blood-retinal barrier." Science Advances 6, no. 35 (August 2020): eaba7457. http://dx.doi.org/10.1126/sciadv.aba7457.

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Breakdown of the blood-retinal barrier (BRB) causes retinal edema and vision loss. We investigated the role of Wnt signaling in maintaining the BRB by limiting transcytosis. Mice lacking either the Wnt co-receptor low-density lipoprotein receptor–related protein 5 (Lrp5−/−) or the Wnt ligand Norrin (Ndpy/−) exhibit increased retinal vascular leakage and enhanced endothelial transcytosis. Wnt signaling directly controls the transcription of an endothelium-specific transcytosis inhibitor, major facilitator superfamily domain–containing protein 2a (MFSD2A), in a β-catenin–dependent manner. MFSD2A overexpression reverses Wnt deficiency–induced transcytosis in endothelial cells and in retinas. Moreover, Wnt signaling mediates MFSD2A-dependent vascular endothelium transcytosis through a caveolin-1 (CAV-1)–positive caveolae pathway. In addition, levels of omega-3 fatty acids are also decreased in Wnt signaling–deficient retinas, reflecting the basic function of MFSD2A as a lipid transporter. Our findings uncovered the Wnt/β-catenin/MFSD2A/CAV-1 axis as a key pathway governing endothelium transcytosis and inner BRB integrity.

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16

Zhou, Jinhua, and Zhenggao Xie. "Endostatin Inhibits Blood-Retinal Barrier Breakdown in Diabetic Rats by Increasing the Expression of ICAM-1 and VCAM-1 and Decreasing the Expression of VEGF." Computational and Mathematical Methods in Medicine 2022 (January 17, 2022): 1–9. http://dx.doi.org/10.1155/2022/5105866.

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Objective. Endostatin has become the strongest endogenous angiogenesis inhibitor due to suppressing VEGF expression. The purpose of this study was to assess the impact of endostatin on the blood-retinal barrier (BRB) in diabetic rats. Methods. SD rats were induced to develop diabetes by streptozotocin, and endostatin was administrated by intravitreal injection. The body weight, the level of blood glucose, the expressions of C-reactive protein (CRP), adhesion molecules intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), junction proteins (occludin, claudin-5, and zonula occluden-1), and VEGF were measured in rats’ retinas of diabetes. The BRB breakdown was evaluated using Evans blue. Results. The level of CRP and adhesion molecules (ICAM-1 and VCAM-1) was increased in retinas of diabetic rats, while endostatin significantly inhibited the upregulation of these. Diabetes increased the BRB permeability and retinal thickness. Diabetes also decreased the levels of occludin, claudin-5, and ZO-1 in retinals. These changes were inhibited by endostatin treatment. Upregulation of vascular endothelial growth factor (VEGF), transforming growth factor-β (TGF-β), and protein kinase C- (PKC-) β2 was also reversed by endostatin in retinas of diabetic rats. Conclusions. Endostatin provides protection against diabetic retinopathy, which may involve its barrier-enhancing effects.

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17

Wilson, Charles A., Bruce A. Berkowitz, Hideharu Funatsu, David C. Metrikin, David W. Harrison, Michael K. Lam, and Peter L. Sonkin. "Blood-retinal barrier breakdown following experimental retinal ischemia and reperfusion." Experimental Eye Research 61, no. 5 (November 1995): 547–57. http://dx.doi.org/10.1016/s0014-4835(05)80048-x.

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18

Hosoya, Ken-ichi, and Masanori Tachikawa. "Inner Blood-Retinal Barrier Transporters: Role of Retinal Drug Delivery." Pharmaceutical Research 26, no. 9 (July 1, 2009): 2055–65. http://dx.doi.org/10.1007/s11095-009-9930-2.

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19

Cai, Siwei, Qianhui Yang, Mengzhu Hou, Qian Han, Hanyu Zhang, Jiantao Wang, Chen Qi, et al. "Α-Melanocyte-Stimulating Hormone Protects Early Diabetic Retina from Blood-Retinal Barrier Breakdown and Vascular Leakage via MC4R." Cellular Physiology and Biochemistry 45, no. 2 (2018): 505–22. http://dx.doi.org/10.1159/000487029.

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Background/Aims: Blood-retinal barrier (BRB) breakdown and vascular leakage is the leading cause of blindness of diabetic retinopathy (DR). Hyperglycemia-induced oxidative stress and inflammation are primary pathogenic factors of this severe DR complication. An effective interventional modality against the pathogenic factors during early DR is needed to curb BRB breakdown and vascular leakage. This study sought to examine the protective effects of α-Melanocyte-stimulating hormone (α-MSH) on early diabetic retina against vascular hyperpermeability, electrophysiological dysfunction, and morphological deterioration in a rat model of diabetes and probe the mechanisms underlying the α-MSH’s anti-hyperpermeability in both rodent retinas and simian retinal vascular endothelial cells (RF6A). Methods: Sprague Dawley rats were injected through tail vein with streptozotocin to induce diabetes. The rats were intravitreally injected with α-MSH or saline at Week 1 and 3 after hyperglycemia. In another 2 weeks, Evans blue assay, transmission electron microscopy, electroretinogram (ERG), and hematoxylin and eosin (H&E) staining were performed to examine the protective effects of α-MSH in diabetic retinas. The expression of pro-inflammatory factors and tight junction at mRNA and protein levels in retinas was analyzed. Finally, the α-MSH’s anti-hyperpermeability was confirmed in a high glucose (HG)-treated RF6A cell monolayer transwell culture by transendothelial electrical resistance (TEER) measurement and a fluorescein isothiocyanate-Dextran assay. Universal or specific melanocortin receptor (MCR) blockers were also employed to elucidate the MCR subtype mediating α-MSH’s protection. Results: Evans blue assay showed that BRB breakdown and vascular leakage was detected, and rescued by α-MSH both qualitatively and quantitatively in early diabetic retinas; electron microscopy revealed substantially improved retinal and choroidal vessel ultrastructures in α-MSH-treated diabetic retinas; scotopic ERG suggested partial rescue of functional defects by α-MSH in diabetic retinas; and H&E staining revealed significantly increased thickness of all layers in α-MSH-treated diabetic retinas. Mechanistically, α-MSH corrected aberrant transcript and protein expression of pro-inflammatory factor and tight junction genes in the diseased retinas; moreover, it prevented abnormal changes in TEER and permeability in HG-stimulated RF6A cells, and this anti-hyperpermeability was abolished by a universal MCR blocker or an antagonist specific to MC4R. Conclusions: This study showed previously undescribed protective effects of α-MSH on inhibiting BRB breakdown and vascular leakage, improving electrophysiological functions and morphology in early diabetic retinas, which may be due to its down-regulating pro-inflammatory factors and augmenting tight junctions. α-MSH acts predominantly on MC4R to antagonize hyperpermeability in retinal microvessel endothelial cells.

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20

PULIDO, JOSE S., and NORMAN P. BLAIR. "THE BLOOD-RETINAL BARRIER IN BERLINʼS EDEMA." Retina 7, no. 4 (1987): 233–36. http://dx.doi.org/10.1097/00006982-198707040-00007.

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21

KORTE, GARY E., MARGARET S. BURNS, and ROY BELLHORN. "Experimental Manipulation of the Blood-Retinal Barrier." Annals of the New York Academy of Sciences 529, no. 1 Fourth Colloq (June 1988): 106–10. http://dx.doi.org/10.1111/j.1749-6632.1988.tb51433.x.

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22

Coburn, Phillip S., Brandt J. Wiskur, Roger A. Astley, and Michelle C. Callegan. "Blood–Retinal Barrier Compromise and EndogenousStaphylococcus aureusEndophthalmitis." Investigative Opthalmology & Visual Science 56, no. 12 (November 11, 2015): 7303. http://dx.doi.org/10.1167/iovs.15-17488.

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23

Bernardes, R., J. Dias, and J. Cunha-Vaz. "Mapping the Human Blood-Retinal Barrier Function." IEEE Transactions on Biomedical Engineering 52, no. 1 (January 2005): 106–16. http://dx.doi.org/10.1109/tbme.2004.839801.

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24

Brown, R., and M. F. Raines. "The blood-retinal barrier in angioid streaks." Eye 2, no. 5 (September 1988): 547–51. http://dx.doi.org/10.1038/eye.1988.105.

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25

MANNERMAA, E., KS VELLONEN, T. RYHÄNEN, K. KAARNIRANTA, and A. URTTI. "Efflux proteins of outer blood-retinal barrier." Acta Ophthalmologica Scandinavica 85 (October 2, 2007): 0. http://dx.doi.org/10.1111/j.1600-0420.2007.01063_3238.x.

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26

Yoshida, Akitoshi, Satoshi Ishiko, and Mitsuru Kojima. "Outward permeability of the blood-retinal barrier." Graefe's Archive for Clinical and Experimental Ophthalmology 230, no. 1 (January 1992): 78–83. http://dx.doi.org/10.1007/bf00166767.

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27

Archer, D. B., T. A. Gardiner, and N. K. Sharma. "The inner blood-retinal barrier in diabetes." Graefe's Archive for Clinical and Experimental Ophthalmology 222, no. 4-5 (February 1985): 186–88. http://dx.doi.org/10.1007/bf02133671.

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28

Kang, Min-Kyung, Dongyeon Kim, and Young-Hee Kang. "Protective Effect of Nobiletin on High Glucose-Induced Blood-Retinal Barrier (BRB) Breakdown." Current Developments in Nutrition 5, Supplement_2 (June 2021): 25. http://dx.doi.org/10.1093/cdn/nzab033_025.

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Abstract Objectives Diabetic retinopathy (DR) is a complication of diabetes, caused by high blood glucose levels damaging to blood vessels in the retina. It can leading cause of blindness. Nobiletin is a polymethoxyflavone present in citrus fruit and peels, it has anti-cancer and anti-inflammatory effects. This study investigated the protective effects of nobiletin on retinal blood-retinal barrier (BRB) breakdown in high glucose-exposed human retinal endothelial cells and in db/db mouse eyes. Methods Human retinal microvascular endothelial cell (HRMVEC) were incubated in media exposed to 33 mM glucose in the absence and presence of 1–20 μM nobiletin up to 5 d. Antibodies ZO-1, MMP2, Bax and Bcl2 were used for western blot analysis. The in vivo animal model employed db/db mice orally administrated with 10 mg/kg of nobiletin. Results Non-toxic nobiletin declined the expression of ZO-1 which is retinal tight junction protein and Bcl2 expression in high glucose stimulation. when treated with nobiletin promoted the expression of ZO-1 and Bcl2 in HRMVEC cell. Also, of MMP2 and Bax was up-regulated by high glucose stimulation and nobiletin down-regulated high glucose induced expression of the MMP2 and Bax. In in vivo study, oral administration of 10 mg/kg nobiletin protected the retinal endothelial microvascular through recovering ZO-1 and Bcl2 expression as control. Also, nobiletin reduced tissue expressions of MMP2 and Bax. Conclusions These results demonstrated that nobiletin may be a potent retinoprotective agent to prevent diabetes-associated microvascular abnormalities and BRB breakdown in retinal microvascular functions leading to retinal failure. Funding Sources This work was supported by the National Research Foundation of Korea (NRF) grants funded by the Korea government (2017R1A6A3A04011473).

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29

Reichhart, Nadine, Nadine Haase, Sergio Crespo-Garcia, Sergej Skosyrski, Christina Herrspiegel, Norbert Kociok, Rudolf Fuchshofer, et al. "Hypertensive retinopathy in a transgenic angiotensin-based model." Clinical Science 130, no. 13 (May 23, 2016): 1075–88. http://dx.doi.org/10.1042/cs20160092.

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Severe hypertension destroys eyesight. The RAS (renin–angiotensin system) may contribute to this. This study relied on an established angiotensin, AngII (angiotensin II)-elevated dTGR (double-transgenic rat) model and same-background SD (Sprague–Dawley) rat controls. In dTGRs, plasma levels of AngII were increased. We determined the general retinal phenotype and observed degeneration of ganglion cells that we defined as vascular degeneration. We also inspected relevant gene expression and lastly observed alterations in the outer blood–retinal barrier. We found that both scotopic a-wave and b-wave as well as oscillatory potential amplitude were significantly decreased in dTGRs, compared with SD rat controls. However, the b/a-wave ratio remained unchanged. Fluorescence angiography of the peripheral retina indicated that exudates, or fluorescein leakage, from peripheral vessels were increased in dTGRs compared with controls. Immunohistological analysis of blood vessels in retina whole-mount preparations showed structural alterations in the retina of dTGRs. We then determined the general retinal phenotype. We observed the degeneration of ganglion cells, defined vascular degenerations and finally found differential expression of RAS-related genes and angiogenic genes. We found the expression of both human angiotensinogen and human renin in the hypertensive retina. Although the renin gene expression was not altered, the AngII levels in the retina were increased 4-fold in the dTGR retina compared with that in SD rats, a finding with mechanistic implications. We suggest that alterations in the outer blood–retinal barrier could foster an area of visual-related research based on our findings. Finally, we introduce the dTGR model of retinal disease.

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30

Sharma, Deepti, Geetika Kaur, Shivantika Bisen, Anamika Sharma, Ahmed S. Ibrahim, and Nikhlesh K. Singh. "IL-33 via PKCμ/PRKD1 Mediated α-Catenin Phosphorylation Regulates Endothelial Cell-Barrier Integrity and Ischemia-Induced Vascular Leakage." Cells 12, no. 5 (February 23, 2023): 703. http://dx.doi.org/10.3390/cells12050703.

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Angiogenesis, neovascularization, and vascular remodeling are highly dynamic processes, where endothelial cell–cell adhesion within the vessel wall controls a range of physiological processes, such as growth, integrity, and barrier function. The cadherin–catenin adhesion complex is a key contributor to inner blood–retinal barrier (iBRB) integrity and dynamic cell movements. However, the pre-eminent role of cadherins and their associated catenins in iBRB structure and function is not fully understood. Using a murine model of oxygen-induced retinopathy (OIR) and human retinal microvascular endothelial cells (HRMVECs), we try to understand the significance of IL-33 on retinal endothelial barrier disruption, leading to abnormal angiogenesis and enhanced vascular permeability. Using electric cell-substrate impedance sensing (ECIS) analysis and FITC-dextran permeability assay, we observed that IL-33 at a 20 ng/mL concentration induced endothelial-barrier disruption in HRMVECs. The adherens junction (AJs) proteins play a prominent role in the selective diffusion of molecules from the blood to the retina and in maintaining retinal homeostasis. Therefore, we looked for the involvement of adherens junction proteins in IL-33-mediated endothelial dysfunction. We observed that IL-33 induces α-catenin phosphorylation at serine/threonine (Ser/Thr) residues in HRMVECs. Furthermore, mass-spectroscopy (MS) analysis revealed that IL-33 induces the phosphorylation of α-catenin at Thr654 residue in HRMVECs. We also observed that PKCμ/PRKD1-p38 MAPK signaling regulates IL-33-induced α-catenin phosphorylation and retinal endothelial cell-barrier integrity. Our OIR studies revealed that genetic deletion of IL-33 resulted in reduced vascular leakage in the hypoxic retina. We also observed that the genetic deletion of IL-33 reduced OIR-induced PKCμ/PRKD1-p38 MAPK-α-catenin signaling in the hypoxic retina. Therefore, we conclude that IL-33-induced PKCμ/PRKD1-p38 MAPK-α-catenin signaling plays a significant role in endothelial permeability and iBRB integrity.

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31

Bunt-Milam, Ann H., Richard A. Black, and Richard E. Bensinger. "Breakdown of the outer blood-retinal barrier in experimental Commotio retinae." Experimental Eye Research 43, no. 3 (September 1986): 397–412. http://dx.doi.org/10.1016/s0014-4835(86)80076-8.

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32

Beach, Krista M., Jianbo Wang, and Deborah C. Otteson. "Regulation of Stem Cell Properties of Müller Glia by JAK/STAT and MAPK Signaling in the Mammalian Retina." Stem Cells International 2017 (2017): 1–15. http://dx.doi.org/10.1155/2017/1610691.

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In humans and other mammals, the neural retina does not spontaneously regenerate, and damage to the retina that kills retinal neurons results in permanent blindness. In contrast to embryonic stem cells, induced pluripotent stem cells, and embryonic/fetal retinal stem cells, Müller glia offer an intrinsic cellular source for regenerative strategies in the retina. Müller glia are radial glial cells within the retina that maintain retinal homeostasis, buffer ion flux associated with phototransduction, and form the blood/retinal barrier within the retina proper. In injured or degenerating retinas, Müller glia contribute to gliotic responses and scar formation but also show regenerative capabilities that vary across species. In the mammalian retina, regenerative responses achieved to date remain insufficient for potential clinical applications. Activation of JAK/STAT and MAPK signaling by CNTF, EGF, and FGFs can promote proliferation and modulate the glial/neurogenic switch. However, to achieve clinical relevance, additional intrinsic and extrinsic factors that restrict or promote regenerative responses of Müller glia in the mammalian retina must be identified. This review focuses on Müller glia and Müller glial-derived stem cells in the retina and phylogenetic differences among model vertebrate species and highlights some of the current progress towards understanding the cellular mechanisms regulating their regenerative response.

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Stofkova, Andrea, Miloslav Zloh, Dominika Andreanska, Ivana Fiserova, Jan Kubovciak, Jan Hejda, Patrik Kutilek, and Masaaki Murakami. "Depletion of Retinal Dopaminergic Activity in a Mouse Model of Rod Dysfunction Exacerbates Experimental Autoimmune Uveoretinitis: A Role for the Gateway Reflex." International Journal of Molecular Sciences 23, no. 1 (December 31, 2021): 453. http://dx.doi.org/10.3390/ijms23010453.

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The gateway reflex is a mechanism by which neural inputs regulate chemokine expression at endothelial cell barriers, thereby establishing gateways for the invasion of autoreactive T cells into barrier-protected tissues. In this study, we hypothesized that rod photoreceptor dysfunction causes remodeling of retinal neural activity, which influences the blood–retinal barrier and the development of retinal inflammation. We evaluated this hypothesis using Gnat1rd17 mice, a model of night blindness with late-onset rod-cone dystrophy, and experimental autoimmune uveoretinitis (EAU). Retinal remodeling and its effect on EAU development were investigated by transcriptome profiling, target identification, and functional validation. We showed that Gnat1rd17 mice primarily underwent alterations in their retinal dopaminergic system, triggering the development of an exacerbated EAU, which was counteracted by dopamine replacement with L-DOPA administered either systemically or locally. Remarkably, dopamine acted on retinal endothelial cells to inhibit NF-κB and STAT3 activity and the expression of downstream target genes such as chemokines involved in T cell recruitment. These results suggest that rod-mediated dopamine release functions in a gateway reflex manner in the homeostatic control of immune cell entry into the retina, and the loss of retinal dopaminergic activity in conditions associated with rod dysfunction increases the susceptibility to autoimmune uveitis.

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Kim, Jin Hyoung, Jeong Hun Kim, You Mie Lee, Eun-Mi Ahn, Kyu-Won Kim, and Young Suk Yu. "Decursin Inhibits VEGF-Mediated Inner Blood—Retinal Barrier Breakdown by Suppression of VEGFR-2 Activation." Journal of Cerebral Blood Flow & Metabolism 29, no. 9 (June 17, 2009): 1559–67. http://dx.doi.org/10.1038/jcbfm.2009.78.

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The blood—retinal barrier (BRB) is essential for the normal structural and functional integrity of the retina, whose breakdown could cause the serious vision loss. Vascular endothelial growth factor (VEGF), as a permeable factor, induces alteration of tight junction proteins to result in BRB breakdown. Herein, we demonstrated that decursin inhibits VEGF-mediated inner BRB breakdown through suppression of VEGFR-2 signaling pathway. In retinal endothelial cells, decursin inhibited VEGF-mediated hyperpermeability. Decursin prevented VEGF-mediated loss of tight junction proteins including zonula occludens-1 (ZO-1), ZO-2, and occludin in retinal endothelial cells, which was also supported by restoration of tight junction proteins in intercellular junction. In addition, decursin significantly inhibited VEGF-mediated vascular leakage from retinal vessels, which was accompanied by prevention of loss of tight junction proteins in retinal vessels. Decursin significantly suppressed VEGF-induced VEGFR-2 phosphrylation that consequently led to inhibition of extracellular signal-regulated kinase (ERK) 1/2 activation. Moreover, decursin induced no cytotoxicity to retinal endothelial cells and no retinal toxicity under therapeutic concentrations. Therefore, our results suggest that decursin prevents VEGF-mediated BRB breakdown through blocking of loss of tight junction proteins, which might be regulated by suppression of VEGFR-2 activation. As a novel inhibitor to BRB breakdown, decursin could be applied to variable retinopathies with BRB breakdown.

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Fresta, Claudia G., Annamaria Fidilio, Giuseppe Caruso, Filippo Caraci, Frank J. Giblin, Gian Marco Leggio, Salvatore Salomone, Filippo Drago, and Claudio Bucolo. "A New Human Blood–Retinal Barrier Model Based on Endothelial Cells, Pericytes, and Astrocytes." International Journal of Molecular Sciences 21, no. 5 (February 27, 2020): 1636. http://dx.doi.org/10.3390/ijms21051636.

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Blood–retinal barrier (BRB) dysfunction represents one of the most significant changes occurring during diabetic retinopathy. We set up a high-reproducible human-based in vitro BRB model using retinal pericytes, retinal astrocytes, and retinal endothelial cells in order to replicate the human in vivo environment with the same numerical ratio and layer order. Our findings showed that high glucose exposure elicited BRB breakdown, enhanced permeability, and reduced the levels of junction proteins such as ZO-1 and VE-cadherin. Furthermore, an increased expression of pro-inflammatory mediators (IL-1β, IL-6) and oxidative stress-related enzymes (iNOS, Nox2) along with an increased production of reactive oxygen species were observed in our triple co-culture paradigm. Finally, we found an activation of immune response-regulating signaling pathways (Nrf2 and HO-1). In conclusion, the present model mimics the closest human in vivo milieu, providing a valuable tool to study the impact of high glucose in the retina and to develop novel molecules with potential effect on diabetic retinopathy.

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Zhou, Jiehao, Shikun He, Ning Zhang, Christine Spee, Peng Zhou, Stephen J. Ryan, Ram Kannan, and David R. Hinton. "Neutrophils Compromise Retinal Pigment Epithelial Barrier Integrity." Journal of Biomedicine and Biotechnology 2010 (2010): 1–10. http://dx.doi.org/10.1155/2010/289360.

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We hypothesized that neutrophils and their secreted factors mediate breakdown of the integrity of the outer blood-retina-barrier by degrading the apical tight junctions of the retinal pigment epithelium (RPE). The effect of activated neutrophils or neutrophil cell lysate on apparent permeability of bovine RPE-Choroid explants was evaluated by measuring[H]mannitol flux in a modified Ussing chamber. The expression of matrix metalloproteinase- (MMP-) 9 in murine peritoneal neutrophils, and the effects of neutrophils on RPE tight-junction protein expression were assessed by confocal microscopy and western blot. Our results revealed that basolateral incubation of explants with neutrophils decreased occludin and ZO-1 expression at 1 and 3 hours and increased the permeability of bovine RPE-Choroid explants by >3-fold (P<.05). Similarly, basolateral incubation of explants with neutrophil lysate decreased ZO-1 expression at 1 and 3 hours (P<.05) and increased permeability of explants by 75%. Further, we found that neutrophils prominently express MMP-9 and that incubation of explants with neutrophils in the presence of anti-MMP-9 antibody inhibited the increase in permeability. These data suggest that neutrophil-derived MMP-9 may play an important role in disrupting the integrity of the outer blood-retina barrier.

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Kubo, Yoshiyuki, Shizuka Yahata, Satoshi Miki, Shin-ichi Akanuma, and Ken-ichi Hosoya. "Blood-to-retina transport of riboflavin via RFVTs at the inner blood-retinal barrier." Drug Metabolism and Pharmacokinetics 32, no. 1 (February 2017): 92–99. http://dx.doi.org/10.1016/j.dmpk.2016.09.006.

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Sedwick, Lyn A., Birch MK, Barbosa S, Blumhardt LD, O??Brien C, and Harding SP. "Retinal Venous Sheathing and the Blood-Retinal Barrier in Multiple Sclerosis." Journal of Neuro-Ophthalmology 16, no. 4 (December 1996): 297. http://dx.doi.org/10.1097/00041327-199612000-00018.

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Sellner, PA. "The blood-retinal barrier: leucine transport by the retinal pigment epithelium." Journal of Neuroscience 6, no. 10 (October 1, 1986): 2823–28. http://dx.doi.org/10.1523/jneurosci.06-10-02823.1986.

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Chahal, P. S., T. J. Fallon, and E. M. Kohner. "Measurement of Blood-Retinal Barrier Function in Central Retinal Vein Occlusion." Archives of Ophthalmology 104, no. 4 (April 1, 1986): 554–57. http://dx.doi.org/10.1001/archopht.1986.01050160110024.

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Birch, Michael K. "Retinal Venous Sheathing and the Blood-Retinal Barrier in Multiple Sclerosis." Archives of Ophthalmology 114, no. 1 (January 1, 1996): 34. http://dx.doi.org/10.1001/archopht.1996.01100130032005.

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Collin, Gayle B., Lanying Shi, Minzhong Yu, Nurten Akturk, Jeremy R. Charette, Lillian F. Hyde, Sonia M. Weatherly, et al. "A Splicing Mutation in Slc4a5 Results in Retinal Detachment and Retinal Pigment Epithelium Dysfunction." International Journal of Molecular Sciences 23, no. 4 (February 17, 2022): 2220. http://dx.doi.org/10.3390/ijms23042220.

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Fluid and solute transporters of the retinal pigment epithelium (RPE) are core components of the outer blood–retinal barrier. Characterizing these transporters and their role in retinal homeostasis may provide insights into ocular function and disease. Here, we describe RPE defects in tvrm77 mice, which exhibit hypopigmented patches in the central retina. Mapping and nucleotide sequencing of tvrm77 mice revealed a disrupted 5’ splice donor sequence in Slc4a5, a sodium bicarbonate cotransporter gene. Slc4a5 expression was reduced 19.7-fold in tvrm77 RPE relative to controls, and alternative splice variants were detected. SLC4A5 was localized to the Golgi apparatus of cultured human RPE cells and in apical and basal membranes. Fundus imaging, optical coherence tomography, microscopy, and electroretinography (ERG) of tvrm77 mice revealed retinal detachment, hypopigmented patches corresponding to neovascular lesions, and retinal folds. Detachment worsened and outer nuclear layer thickness decreased with age. ERG a- and b-wave response amplitudes were initially normal but declined in older mice. The direct current ERG fast oscillation and light peak were reduced in amplitude at all ages, whereas other RPE-associated responses were unaffected. These results link a new Slc4a5 mutation to subretinal fluid accumulation and altered light-evoked RPE electrophysiological responses, suggesting that SLC4A5 functions at the outer blood–retinal barrier.

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Kim, Jeong Hun, Jin Hyoung Kim, Young Suk Yu, Chang Sik Cho, and Kyu-Won Kim. "Blockade of Angiotensin II Attenuates VEGF-Mediated Blood—Retinal Barrier Breakdown in Diabetic Retinopathy." Journal of Cerebral Blood Flow & Metabolism 29, no. 3 (December 24, 2008): 621–28. http://dx.doi.org/10.1038/jcbfm.2008.154.

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Diabetic retinopathy (DR) is the leading cause of vision loss as a major complication of diabetes mellitus. The blood—retinal barrier (BRB) breakdown is a critical early event in the pathogenesis of DR. It has been known that the rennin-angiotensin system (RAS) is important in the progression of the DR via angiotensin II (Ang II), the effector of RAS. In this study, we showed that blockade of Ang II attenuates vascular endothelial growth factor (VEGF)-mediated BRB breakdown in DR. In streptozotocin-induced diabetes, retinal vascular permeability increased with upregulation of VEGF, where Ang II and its receptors were upregulated. Ang II induced VEGF expression in retinal endothelial cells accompanied by loss of tight junction proteins. However, the blockade of Ang II by perindopril, an angiotensin converting enzyme (ACE) inhibitor, inhibited upregulation of VEGF, and prevented the loss of tight junction proteins. Moreover, inhibition of Ang II by perindopril attenuated increased vascular permeability of diabetic retina accompanied by recovery of tight junction proteins in retinal vessels. Therefore, we suggest that the RAS involves in increased vascular permeability during early stage of DR, which is mediated by VEGF. Furthermore, the ACE inhibitor may have a therapeutic potential in the treatment of diabetic BRB breakdown.

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BERNARDES, R., P. SERRANHO, P. RODRIGUES, V. GONçALVES, and J. CUNHA‐VAZ. "Blood‐retinal barrier function status from OCT data." Acta Ophthalmologica 89, s248 (September 2011): 0. http://dx.doi.org/10.1111/j.1755-3768.2011.4115.x.

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Molins, Blanca, Adriana Mora, Sara Romero-Vázquez, Anna Pascual-Méndez, Sara Rovira, Marc Figueras-Roca, Mercedes Balcells, Alfredo Adán, and Jordi Martorell. "Shear stress modulates inner blood retinal barrier phenotype." Experimental Eye Research 187 (October 2019): 107751. http://dx.doi.org/10.1016/j.exer.2019.107751.

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Holloway, R. "The blood retinal barrier in diabetes during puberty." Journal of Oral and Maxillofacial Surgery 53, no. 4 (April 1995): 487. http://dx.doi.org/10.1016/0278-2391(95)90735-1.

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KROGSAA, BENT, HENRIK LUND-ANDERSEN, HANS-HENRIK PARVING, and PETER BJAELDAGER. "THE BLOOD-RETINAL BARRIER PERMEABILITY IN ESSENTIAL HYPERTENSION." Acta Ophthalmologica 61, no. 4 (May 27, 2009): 541–44. http://dx.doi.org/10.1111/j.1755-3768.1983.tb04343.x.

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Green, Keith, Tracey Slagle, Manuel J. Chaknis, Lisa Cheeks, and Stanley Chang. "Perfluorocarbon Effects on Rabbit Blood-Retinal Barrier Permeability." Ophthalmic Research 25, no. 3 (1993): 186–91. http://dx.doi.org/10.1159/000267289.

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Howard-Williams, J. R., M. J. Siegel, S. M. Podos, and V. Brown. "Alteration of the Blood-Retinal Barrier by Dipyridamole." Archives of Ophthalmology 104, no. 4 (April 1, 1986): 488–90. http://dx.doi.org/10.1001/archopht.1986.01050160040006.

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de Abreu, José R. Faria. "The Blood-Retinal Barrier in Diabetes During Puberty." Archives of Ophthalmology 112, no. 10 (October 1, 1994): 1334. http://dx.doi.org/10.1001/archopht.1994.01090220084027.

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