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Glenda C. Gobe - One of the best experts on this subject based on the ideXlab platform.
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Vitreal macrophages express vascular endothelial growth factor in Oxygen-Induced Retinopathy.
Clinical & experimental ophthalmology, 2000Co-Authors: Helen L. Naug, Glen A. Gole, Jay Browning, Glenda C. GobeAbstract:Purpose: The possibility of vitreal macrophages playing an angiogenic role in Oxygen-Induced Retinopathy (OIR) was investigated. Oxygen-Induced Retinopathy was produced in newborn animals with the purpose of modeling the proliferative phase of human Retinopathy of prematurity (ROP). Materials and Methods: To produce OIR in neonatal mice, litters at postnatal day 7 were placed in 80-90% oxygen for a period of 5 days and then returned to room air. Pups were killed on days 7, 12, 15, 17 and 20 over the postnatal period and were perfusion-fixed using a saline wash-out, followed by 4% paraformaldehyde and then India Ink. Eyes were enucleated and either whole-mounted, or snap-frozen and cryosectioned. Immunostaining procedures were used to visualize macrophages and vascular endothelial growth factor (VEGF) protein. The primary antibodies used were anti-F4/80 and antimouse VEGF, respectively. Vitreal macrophages closely associated with the vitreo-retinal interface (within 25 mum of the inner limiting membrane) were counted. In situ hybridization procedures were used to analyse for the presence of VEGF mRNA transcript in vitreal macrophages. Results: Macrophage numbers were found to significantly increase (P < 0.05) in eyes from oxygen-treated animals compared with those from age-matched controls. A close spatial relationship was observed between macrophages and vitreal neovascular sprouts. In addition, vitreal macrophages were also found to transcribe and express VEGF in the oxygen-treated animals during the vasoproliferative phase. Conclusions: Our results raise the possibility that vitreal macrophages play a role in the pathogenesis of OIR and by inference, ROP.
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Vitreal macrophages express VEGF in Oxygen-Induced Retinopathy
1998Co-Authors: Helen L. Naug, Glen A. Gole, Jay Browning, Glenda C. GobeAbstract:The possibility that macrophages promote vitreal neovascularization in Oxygen-Induced Retinopathy (OIR) was investigated. OIR describes the disorder displayed in animal models of Retinopathy of prematurity (ROP). Both OIR and ROP are characterised by vascular proliferation within the retina and from the retina into the vitreous gel of the eye. Formation of vitreal neovascular sprouts is the most severe manifestation of the neovascular response. Using immunohistochemistry, we mapped the presence of macrophages and VEGF protein in neonatal mice eyes over the postnatal period. Animals with OIR were compared with age-matched controls. Macrophages were observed in close association with developing vitreal sprouts, and a large proportion of vitreal macrophages were found to express VEGF protein. These findings suggest that macrophages induce the formation of vitreal sprouts in OIR.
Glen A. Gole - One of the best experts on this subject based on the ideXlab platform.
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Vitreal macrophages express vascular endothelial growth factor in Oxygen-Induced Retinopathy.
Clinical & experimental ophthalmology, 2000Co-Authors: Helen L. Naug, Glen A. Gole, Jay Browning, Glenda C. GobeAbstract:Purpose: The possibility of vitreal macrophages playing an angiogenic role in Oxygen-Induced Retinopathy (OIR) was investigated. Oxygen-Induced Retinopathy was produced in newborn animals with the purpose of modeling the proliferative phase of human Retinopathy of prematurity (ROP). Materials and Methods: To produce OIR in neonatal mice, litters at postnatal day 7 were placed in 80-90% oxygen for a period of 5 days and then returned to room air. Pups were killed on days 7, 12, 15, 17 and 20 over the postnatal period and were perfusion-fixed using a saline wash-out, followed by 4% paraformaldehyde and then India Ink. Eyes were enucleated and either whole-mounted, or snap-frozen and cryosectioned. Immunostaining procedures were used to visualize macrophages and vascular endothelial growth factor (VEGF) protein. The primary antibodies used were anti-F4/80 and antimouse VEGF, respectively. Vitreal macrophages closely associated with the vitreo-retinal interface (within 25 mum of the inner limiting membrane) were counted. In situ hybridization procedures were used to analyse for the presence of VEGF mRNA transcript in vitreal macrophages. Results: Macrophage numbers were found to significantly increase (P < 0.05) in eyes from oxygen-treated animals compared with those from age-matched controls. A close spatial relationship was observed between macrophages and vitreal neovascular sprouts. In addition, vitreal macrophages were also found to transcribe and express VEGF in the oxygen-treated animals during the vasoproliferative phase. Conclusions: Our results raise the possibility that vitreal macrophages play a role in the pathogenesis of OIR and by inference, ROP.
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Vitreal macrophages express VEGF in Oxygen-Induced Retinopathy
1998Co-Authors: Helen L. Naug, Glen A. Gole, Jay Browning, Glenda C. GobeAbstract:The possibility that macrophages promote vitreal neovascularization in Oxygen-Induced Retinopathy (OIR) was investigated. OIR describes the disorder displayed in animal models of Retinopathy of prematurity (ROP). Both OIR and ROP are characterised by vascular proliferation within the retina and from the retina into the vitreous gel of the eye. Formation of vitreal neovascular sprouts is the most severe manifestation of the neovascular response. Using immunohistochemistry, we mapped the presence of macrophages and VEGF protein in neonatal mice eyes over the postnatal period. Animals with OIR were compared with age-matched controls. Macrophages were observed in close association with developing vitreal sprouts, and a large proportion of vitreal macrophages were found to express VEGF protein. These findings suggest that macrophages induce the formation of vitreal sprouts in OIR.
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Quantification of Oxygen-Induced Retinopathy in the mouse.
Investigative ophthalmology & visual science, 1997Co-Authors: Jay Browning, Christine K. Wylie, Glen A. GoleAbstract:PURPOSE: To describe a quantifiable model of vascular proliferation in Oxygen-Induced Retinopathy (OIR) in the mouse. METHODS: Neonate Quackenbush mice were subjected to high-ambient oxygen (approximately 95%) for the first 5 days after birth, effecting a total inhibition of retinal vascular growth. Animals then were returned to room air, and the rates of subsequent vascular development in the plane of the retina and estimates of retinal capillary density were measured from flatmounts of ink-perfused eyes. Observations were confirmed with fluorescein isothiocyanate-lectin labeling of the peripheral vasculature. Abnormal growth of vascular sprouts into the vitreous was recorded from cross-sections. Observations in OIR were compared against those of age-matched control animals. RESULTS: The slower rate of retinal revascularization in OIR mice was quantified and compared against the normal rate. Lectin-binding studies confirmed the reliability of ink preparations. The number of vitreous sprouts in OIR peaked 8 to 10 days after animals were returned to room air (13 to 15 postnatal days). Sprouts then regressed, to disappear by postnatal day 20. In all respects, bar a slightly lower peripheral capillary density, the normal retinal vascular pattern was achieved in OIR within 15 days of exposure to room air (as opposed to the 10 days required in control mice). CONCLUSIONS: The protocol described for quantifying retinal proliferation in mouse OIR is reproduced readily, and the data recorded here will allow the effectiveness of subsequent treatments that may affect retinal vascular growth to be evaluated better.
Kay D. Beharry - One of the best experts on this subject based on the ideXlab platform.
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Pharmacologic synergism of ocular ketorolac and systemic caffeine citrate in rat Oxygen-Induced Retinopathy
Pediatric Research, 2016Co-Authors: Jacob V Aranda, Charles L. Cai, Taimur Ahmad, Vadim Bronshtein, Jonathan Sadeh, Gloria B. Valencia, Douglas R. Lazzaro, Kay D. BeharryAbstract:Background: Caffeine or ketorolac decrease the risk of Retinopathy of prematurity and may act synergistically to improve beneficial effect. Combination of caffeine (Caff) and ketorolac (Keto) to prevent Oxygen-Induced Retinopathy was studied. Methods: Newborn rats exposed to room air (RA) or intermittent hypoxia (IH) consisting of 12% O_2 during hyperoxia (50% O_2) from birth (P0) had single daily IP injections of Caff from P0-P13 or saline; and/or ocular Keto (Acuvail, 0.45% ophthalmic solution) administered subcutaneously over the eyes from P5-P7. Pups were studied at P14 or placed in RA for recovery from IH (IHR) until P21. Eyes were examined for neovascularization, histopathology, growth factors, and VEGF-signaling genes. Results: Severe retinal damage noted during IHR in the untreated groups evidenced by hemorrhage, neovascularization, and Oxygen-Induced Retinopathy (OIR) pathologies were prevented with Keto/Caff treatment. Keto and/or Caff treatment in IH also promoted retinal neural development evidenced by eye opening (92%, P < 0.001 vs. 31% in the placebo-treated IH group). No corneal pathologies were noted with Keto. Conclusion. Caff or Keto given individually reduced retinal neovascularization, but the two drugs given together prevented severe OIR.
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Pharmacologic synergism of ocular ketorolac and systemic caffeine citrate in rat Oxygen-Induced Retinopathy.
Pediatric research, 2016Co-Authors: Jacob V Aranda, Charles L. Cai, Taimur Ahmad, Vadim Bronshtein, Jonathan Sadeh, Gloria B. Valencia, Douglas R. Lazzaro, Kay D. BeharryAbstract:Pharmacologic synergism of ocular ketorolac and systemic caffeine citrate in rat Oxygen-Induced Retinopathy
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Hydrogen peroxide accumulation in the choroid during intermittent hypoxia increases risk of severe Oxygen-Induced Retinopathy in neonatal rats.
Investigative ophthalmology & visual science, 2013Co-Authors: Kay D. Beharry, Charles L. Cai, Vadim Bronshtein, Gloria B. Valencia, Douglas R. Lazzaro, Poonam Sharma, Jacob V ArandaAbstract:Purpose. Extremely low gestational age neonates (ELGANs) requiring oxygen therapy often experience frequent episodes of intermittent hypoxia (IH) and are at high risk for severe Retinopathy of prematurity (ROP). Using an established model for Oxygen-Induced Retinopathy (OIR), we examined the hypothesis that there is a critical number of daily brief IH episodes which will result in irreversible retinal oxidative damage.
Jay Browning - One of the best experts on this subject based on the ideXlab platform.
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Vitreal macrophages express vascular endothelial growth factor in Oxygen-Induced Retinopathy.
Clinical & experimental ophthalmology, 2000Co-Authors: Helen L. Naug, Glen A. Gole, Jay Browning, Glenda C. GobeAbstract:Purpose: The possibility of vitreal macrophages playing an angiogenic role in Oxygen-Induced Retinopathy (OIR) was investigated. Oxygen-Induced Retinopathy was produced in newborn animals with the purpose of modeling the proliferative phase of human Retinopathy of prematurity (ROP). Materials and Methods: To produce OIR in neonatal mice, litters at postnatal day 7 were placed in 80-90% oxygen for a period of 5 days and then returned to room air. Pups were killed on days 7, 12, 15, 17 and 20 over the postnatal period and were perfusion-fixed using a saline wash-out, followed by 4% paraformaldehyde and then India Ink. Eyes were enucleated and either whole-mounted, or snap-frozen and cryosectioned. Immunostaining procedures were used to visualize macrophages and vascular endothelial growth factor (VEGF) protein. The primary antibodies used were anti-F4/80 and antimouse VEGF, respectively. Vitreal macrophages closely associated with the vitreo-retinal interface (within 25 mum of the inner limiting membrane) were counted. In situ hybridization procedures were used to analyse for the presence of VEGF mRNA transcript in vitreal macrophages. Results: Macrophage numbers were found to significantly increase (P < 0.05) in eyes from oxygen-treated animals compared with those from age-matched controls. A close spatial relationship was observed between macrophages and vitreal neovascular sprouts. In addition, vitreal macrophages were also found to transcribe and express VEGF in the oxygen-treated animals during the vasoproliferative phase. Conclusions: Our results raise the possibility that vitreal macrophages play a role in the pathogenesis of OIR and by inference, ROP.
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Vitreal macrophages express VEGF in Oxygen-Induced Retinopathy
1998Co-Authors: Helen L. Naug, Glen A. Gole, Jay Browning, Glenda C. GobeAbstract:The possibility that macrophages promote vitreal neovascularization in Oxygen-Induced Retinopathy (OIR) was investigated. OIR describes the disorder displayed in animal models of Retinopathy of prematurity (ROP). Both OIR and ROP are characterised by vascular proliferation within the retina and from the retina into the vitreous gel of the eye. Formation of vitreal neovascular sprouts is the most severe manifestation of the neovascular response. Using immunohistochemistry, we mapped the presence of macrophages and VEGF protein in neonatal mice eyes over the postnatal period. Animals with OIR were compared with age-matched controls. Macrophages were observed in close association with developing vitreal sprouts, and a large proportion of vitreal macrophages were found to express VEGF protein. These findings suggest that macrophages induce the formation of vitreal sprouts in OIR.
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Quantification of Oxygen-Induced Retinopathy in the mouse.
Investigative ophthalmology & visual science, 1997Co-Authors: Jay Browning, Christine K. Wylie, Glen A. GoleAbstract:PURPOSE: To describe a quantifiable model of vascular proliferation in Oxygen-Induced Retinopathy (OIR) in the mouse. METHODS: Neonate Quackenbush mice were subjected to high-ambient oxygen (approximately 95%) for the first 5 days after birth, effecting a total inhibition of retinal vascular growth. Animals then were returned to room air, and the rates of subsequent vascular development in the plane of the retina and estimates of retinal capillary density were measured from flatmounts of ink-perfused eyes. Observations were confirmed with fluorescein isothiocyanate-lectin labeling of the peripheral vasculature. Abnormal growth of vascular sprouts into the vitreous was recorded from cross-sections. Observations in OIR were compared against those of age-matched control animals. RESULTS: The slower rate of retinal revascularization in OIR mice was quantified and compared against the normal rate. Lectin-binding studies confirmed the reliability of ink preparations. The number of vitreous sprouts in OIR peaked 8 to 10 days after animals were returned to room air (13 to 15 postnatal days). Sprouts then regressed, to disappear by postnatal day 20. In all respects, bar a slightly lower peripheral capillary density, the normal retinal vascular pattern was achieved in OIR within 15 days of exposure to room air (as opposed to the 10 days required in control mice). CONCLUSIONS: The protocol described for quantifying retinal proliferation in mouse OIR is reproduced readily, and the data recorded here will allow the effectiveness of subsequent treatments that may affect retinal vascular growth to be evaluated better.
James D. Akula - One of the best experts on this subject based on the ideXlab platform.
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The rat with Oxygen-Induced Retinopathy is myopic with low retinal dopamine.
Investigative ophthalmology & visual science, 2013Co-Authors: Nan Zhang, Ilan Y. Benador, Ronald M. Hansen, Tara L. Favazza, Anne B. Fulton, Anna Maria Baglieri, Emily R. Noonan, P. Michael Iuvone, James D. AkulaAbstract:Purpose. Dopamine (DA) is a neurotransmitter implicated both in modulating neural retinal signals and in eye growth. Therefore, it may participate in the pathogenesis of the most common clinical sequelae of Retinopathy of prematurity (ROP), visual dysfunction and myopia. Paradoxically, in ROP myopia the eye is usually small. The eye of the rat with Oxygen-Induced Retinopathy (OIR) is characterized by retinal dysfunction and short axial length. There have been several investigations of the early maturation of DA in rat retina, but little at older ages, and not in the OIR rat. Therefore, DA, retinal function, and refractive state were investigated in the OIR rat.
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The Neurovascular Relation in Oxygen-Induced Retinopathy
Molecular vision, 2008Co-Authors: James D. Akula, Julie A. Mocko, Ilan Y. Benador, Ronald M. Hansen, Tara L. Favazza, Tanya C. Vyhovsky, Anne B. FultonAbstract:Purpose Longitudinal studies in rat models of Retinopathy of prematurity (ROP) have demonstrated that abnormalities of retinal vasculature and function change hand-in-hand. In the developing retina, vascular and neural structures are under cooperative molecular control. In this study of rats with Oxygen-Induced Retinopathy (OIR) models of ROP, mRNA expression of vascular endothelial growth factor (VEGF), semaphorin (Sema), and their neuropilin receptor (NRP) were examined during the course of Retinopathy to evaluate their roles in the observed neurovascular congruency.
