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1 schemia, neovascularization, and incompetent blood-retinal barrier).
2 ke by glucose in the cells that comprise the blood-retinal barrier.
3 pate in the induction and maintenance of the blood-retinal barrier.
4 rotein activity in cells that form the outer blood-retinal barrier.
5 disorder associated with dysfunction of the blood-retinal barrier.
6 cyte function at sites of a breakdown in the blood-retinal barrier.
7 It can pass the blood-brain barrier and blood-retinal barrier.
8 h OIR, suggesting a protective effect on the blood-retinal barrier.
9 optosis, thereby preserving the integrity of blood-retinal barriers.
10 lly significant increase in breakdown of the blood-retinal barrier (AGE Alb versus Alb, 8.2 vs. 1.6 n
11 n identified as an important mediator of the blood-retinal barrier alteration in diabetic retinopathy
12 localized breakdown in the integrity of the blood-retinal barrier and aberrations in the organizatio
14 role for Mvarphi-derived CD in altering the blood-retinal barrier and reveal a potential therapeutic
15 , which are a crucial component of the outer blood-retinal barrier and the damage is related to retin
16 suggests that there may be breakdown of the blood-retinal barrier and tight junction integrity in a
19 )], pericytes (anti-neural/glial antigen 2), blood-retinal barrier [anti-zonula occludens protein 1 (
20 ve acquired the ability to break through the blood-retinal barrier are thought to be causally involve
21 ecome more important during breakdown of the blood-retinal barrier, as seen after TNF-alpha treatment
22 not bind IGF-1 (IGFBP-3NB), to regulate the blood retinal barrier (BRB) using two distinct experimen
24 Diabetic retinopathy is characterized by blood-retinal barrier (BRB) breakdown and neurotoxicity.
26 kostasis) within the retinal vasculature and blood-retinal barrier (BRB) breakdown and to determine w
29 ial growth factor (VEGF) protein levels, and blood-retinal barrier (BRB) breakdown of the animals wer
30 role of reactive oxygen species (ROS) in the blood-retinal barrier (BRB) breakdown that characterizes
33 sophosphatidylcholine (LPC), are involved in blood-retinal barrier (BRB) damage during diabetic retin
35 lop and characterize a quantitative assay of blood-retinal barrier (BRB) function in mice and to dete
38 studies, functional MRI was used to measure blood-retinal barrier (BRB) integrity after Gd-DTPA inje
42 cular endothelial cells comprising the inner blood-retinal barrier (BRB) is mediated by the GLUT1 glu
43 scular permeability due to alteration of the blood-retinal barrier (BRB) is one of the major complica
45 block vascular permeability and restore the blood-retinal barrier (BRB) may lead to new therapies.
48 f this study was to determine to what extent blood-retinal barrier (BRB) permeability occurred during
58 ffected by hyperglycemia simultaneously with blood retinal barrier breakdown, suggesting that glial a
59 ular endothelial cell injury, apoptosis, and blood-retinal barrier breakdown (P<0.0001) but did not d
60 adhesion molecule-1 (ICAM-1) and results in blood-retinal barrier breakdown and capillary nonperfusi
61 receptor apoptosis, vascular telangiectasis, blood-retinal barrier breakdown and, later, intraretinal
62 IF-1alpha and VEGF increases and the related blood-retinal barrier breakdown are suppressed by inhibi
63 oteinases (MMPs) as a potential cause of the blood-retinal barrier breakdown at the onset of angiogen
64 drops significantly reduced leukostasis and blood-retinal barrier breakdown in a dose-dependent mann
70 ry cytokines that initiate neuronal loss and blood-retinal barrier breakdown seen in diabetic retinop
71 y produces a transient worsening of diabetic blood-retinal barrier breakdown via an HIF-1alpha-mediat
77 circulation with an anti-platelet antibody, blood-retinal barrier breakdown worsened in the diabetic
78 rrent study, diabetic vascular permeability (blood-retinal barrier breakdown) is demonstrated to resu
79 elial growth factor (VEGF) triggers diabetic blood-retinal barrier breakdown, and (2) identify the si
80 n apoptosis, oxidative stress, inflammation, blood-retinal barrier breakdown, and neuroprotection.
81 iabetic retinal vasculature results in early blood-retinal barrier breakdown, capillary nonperfusion,
82 the diabetic retinal vasculature results in blood-retinal barrier breakdown, capillary nonperfusion,
83 adhesion molecule-1 levels, leukostasis, and blood-retinal barrier breakdown, in a relevant animal mo
84 sening of diabetic retinopathy, specifically blood-retinal barrier breakdown, that follows the instit
96 xtracted and assayed for leukocyte adhesion; blood-retinal barrier breakdown; VEGF, TNF-alpha, IL-1be
97 etinopathy increases the permeability of the blood-retinal barrier, but the specific vessels that bec
98 TGF-beta may contribute to breakdown of the blood-retinal barrier by stimulating endothelial cell MM
99 racteristics of tight junctions in the outer blood-retinal barrier change during embryonic developmen
105 diabetic retinopathy and macular edema, the blood-retinal barrier fails to function properly, and th
110 in the cells comprising the inner and outer blood-retinal barriers: human retinal pigment epithelial
114 l pigmented epithelium (RPE) forms the outer blood-retinal barrier in the eye and its polarity is res
119 helium (RPE), which helps maintain the outer blood-retinal barrier, is a local source for ET-1 and wh
120 cations of diabetes is the alteration of the blood-retinal barrier, leading to retinal edema and cons
121 A may have a protective effect against outer blood-retinal barrier leakage associated with diabetic r
122 tein, the vitreous-plasma protein ratio, and blood-retinal barrier leakage by 3-, 1.7-, 3.1-, and 2.7
125 , but transporters for DHA uptake across the blood-retinal barrier or retinal pigment epithelium have
126 ansport, phagocytosis and formation of outer blood-retinal barrier, or possible involvement of JN exp
128 hese results suggest that astrocytes enhance blood-retinal barrier properties, at least in part by in
129 rowth factor (VEGF)-induced breakdown of the blood-retinal barrier requires protein kinase C (PKC)bet
130 in ICAM-1, leukostasis, and breakdown of the blood-retinal barrier, suggesting that NOX2 is primarily
131 igmented epithelial (RPE) cells maintain the blood-retinal barrier, sustain retinal photoreceptor cel
132 d Fpn is expressed in cells constituting the blood-retinal barrier, the authors tested whether the re
133 lay important roles in the alteration of the blood-retinal barrier through proteolytic degradation of
135 protein [anti-GFAP]) and to investigate the blood-retinal barrier using the tight junction markers z
136 onditions in the subretinal space, the outer blood-retinal barrier was disrupted by compromising reti
138 esis during development and formation of the blood-retinal barrier, which is linked to significant do
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