Induction and Readout of Oxygen-Induced Retinopathy

2019 ◽  
pp. 179-191
Author(s):  
Raffael Liegl ◽  
Claudia Priglinger ◽  
Andreas Ohlmann
Keyword(s):  
Oxygen Induced Retinopathy

scholarly journals TLR2 signaling contributes to the angiogenesis of oxygen-induced retinopathy

2021 ◽  
pp. 108716
Author(s):  
Yuying Sun ◽  
Yao Ni ◽  
Ning Kong ◽  
Chunyu Huang
Keyword(s):  
Oxygen Induced Retinopathy ◽  
Tlr2 Signaling

Anti-apoptotic effect of interleukin-17 in a mouse model of oxygen-induced retinopathy

2019 ◽  
Vol 187 ◽  
pp. 107743 ◽  
Author(s):  
Na Li ◽  
Sha Gao ◽  
Jing Wang ◽  
Yanji Zhu ◽  
Xi Shen
Keyword(s):  
Mouse Model ◽  
Interleukin 17 ◽  
Oxygen Induced Retinopathy ◽  
Apoptotic Effect

scholarly journals Role of thromboxane in retinal microvascular degeneration in oxygen-induced retinopathy

2001 ◽  
Vol 90 (6) ◽  
pp. 2279-2288 ◽  
Author(s):  
Martin H. Beauchamp ◽  
Ana Katherine Martinez-Bermudez ◽  
Fernand Gobeil ◽  
Anne Marilise Marrache ◽  
Xin Hou ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Endothelial Cell ◽  
Oxidant Stress ◽  
Microvascular Endothelial Cell ◽  
Oxygen Induced Retinopathy ◽  
Rat Pups ◽  
Endothelial Cell Death ◽  
Peroxidation Product ◽  
Synthase Inhibitor

Microvascular degeneration is an important event in oxygen-induced retinopathy (OIR), a model of retinopathy of prematurity. Because oxidant stress abundantly generates thromboxane A2(TxA2), we tested whether TxA2plays a role in retinal vasoobliteration of OIR and contributes to such vascular degeneration by direct endothelial cytotoxicity. Hyperoxia-induced retinal vasoobliteration in rat pups (80% O2exposure from postnatal days 5–14) was associated with increased TxB2generation and was significantly prevented by TxA2synthase inhibitor CGS-12970 (10 mg · kg−1· day−1) or TxA2-receptor antagonist CGS-22652 (10 mg · kg−1· day−1). TxA2mimetics U-46619 (EC5050 nM) and I-BOP (EC505 nM) caused a time- and concentration-dependent cell death of neuroretinovascular endothelial cells from rats as well as newborn pigs but not of smooth muscle and astroglial cells; other prostanoids did not cause cell death. The peroxidation product 8-iso-PGF2, which is generated in OIR, stimulated TxA2formation by endothelial cells and triggered cell death; these effects were markedly diminished by CGS-12970. TxA2-dependent neuroretinovascular endothelial cell death was mostly by necrosis and to a lesser extent by apoptosis. The data identify an important role for TxA2in vasoobliteration of OIR and unveil a so far unknown function for TxA2in directly triggering neuroretinal microvascular endothelial cell death. These effects of TxA2might participate in other ischemic neurovascular injuries.

scholarly journals A PEDF-Derived Peptide Inhibits Retinal Neovascularization and Blocks Mobilization of Bone Marrow-Derived Endothelial Progenitor Cells

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Richard Longeras ◽  
Krysten Farjo ◽  
Michael Ihnat ◽  
Jian-Xing Ma
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Pigment Epithelium ◽  
Retinal Neovascularization ◽  
Endothelial Progenitor ◽  
Amino Acid Peptide ◽  
Oxygen Induced Retinopathy ◽  
Pigment Epithelium Derived Factor ◽  
Circulating Endothelial Progenitor Cells

Proliferative diabetic retinopathy is characterized by pathological retinal neovascularization, mediated by both angiogenesis (involving mature endothelial cells) and vasculogenesis (involving bone marrow-derived circulating endothelial progenitor cells (EPCs)). Pigment epithelium-derived factor (PEDF) contains an N-terminal 34-amino acid peptide (PEDF-34) that has antiangiogenic properties. Herein, we present a novel finding that PEDF-34 also possesses antivasculogenic activity. In the oxygen-induced retinopathy (OIR) model using transgenic mice that have Tie2 promoter-driven GFP expression, we quantified Tie2GFP+cells in bone marrow and peripheral blood by fluorescence-activated cell sorting (FACS). OIR significantly increased the number of circulating Tie2-GFP+at P16, correlating with the peak progression of neovascularization. Daily intraperitoneal injections of PEDF-34 into OIR mice decreased the number of Tie2-GFP+cells in the circulation at P16 by 65% but did not affect the number of Tie2-GFP+cells in the bone marrow. These studies suggest that PEDF-34 attenuates EPC mobilization from the bone marrow into the blood circulation during retinal neovascularization.

scholarly journals Effect of VEGF Trap on Normal Retinal Vascular Development and Oxygen-Induced Retinopathy in the Dog

2011 ◽  
Vol 52 (7) ◽  
pp. 4039 ◽  
Author(s):  
Gerard A. Lutty ◽  
D. Scott McLeod ◽  
Imran Bhutto ◽  
Stanley J. Wiegand
Keyword(s):  
Vascular Development ◽  
Oxygen Induced Retinopathy ◽  
Vegf Trap

Effects of Marginal Hypoxemia on Recovery from Oxygen-Induced Retinopathy in the Kitten Model

PEDIATRICS ◽  
1984 ◽  
Vol 73 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Dale L. Phelps ◽  
Arthur L. Rosenbaum
Keyword(s):  
Clinical Trials ◽  
Premature Infants ◽  
Vascular Injury ◽  
Retinopathy Of Prematurity ◽  
Oxygen Supplementation ◽  
Predictive Variable ◽  
Oxygen Induced Retinopathy ◽  
Oxygen Administration

Prolonged oxygen administration in premature infants is the most predictive variable for severe retinopathy of prematurity, after degree of prematurity itself. It was noted that infants receiving prolonged oxygen supplementation are probably hypoxemic relative to their healthy counterparts. Therefore, hypoxemia during recovery from a hyperoxic-induced retinal vascular injury was tested in the kitten model of oxygen-induced retinopathy. Twelve litters were exposed to 80% inspired O2 for 65 hours on day 3, and recovered in room air, 13% or 17% oxygen. The retinas were scored at 4 weeks, and 13% oxygen recovery (PO2 = 39 ± 18 torr) was found to worsen significantly the retinopathy compared with that in room air-recovered littermates (P < .01). Hemorrhages occurred more frequently in the retinas from the hypoxemic-recovered kittens. Clinical trials of this hypothesis are indicated in humans.

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