Oxygen-induced retinopathy in the newborn rat: a scoring system for the evaluation of retinal vascular changes

Ricci, Beatrice; Lepore, Domenico; Zonghi, Enrico; Calogero, Giuseppe

doi:10.1007/bf00142683

Cited by 4 publications

(4 citation statements)

References 14 publications

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“…Despite the lack of phenotype in the β-catenin KO mice under normal conditions, the KO mice displayed less severe pathological phenotypes under retinal ischemia and diabetes. OIR is a model of ischemia-induced retinal NV commonly used to study proliferative DR [33] . Its pathology of pre-retinal NV and pathogenesis such as ischemia-induced over-expression of VEGF are similar to those of proliferative DR.…”

Section: Discussionmentioning

confidence: 99%

Interruption of Wnt Signaling in Müller Cells Ameliorates Ischemia-Induced Retinal Neovascularization

Zhou

Benyajati

et al. 2014

PLoS ONE

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Retinal Müller cells are major producers of inflammatory and angiogenic cytokines which contribute to diabetic retinopathy (DR). Over-activation of the Wnt/β-catenin pathway has been shown to play an important pathogenic role in DR. However, the roles of Müller cell-derived Wnt/β-catenin signaling in retinal neovascularization (NV) and DR remain undefined. In the present study, mice with conditional β-catenin knockout (KO) in Müller cells were generated and subjected to oxygen-induced retinopathy (OIR) and streptozotocin (STZ)-induced diabetes. Wnt signaling was evaluated by measuring levels of β-catenin and expression of its target genes using immunoblotting. Retinal vascular permeability was measured using Evans blue as a tracer. Retinal NV was visualized by angiography and quantified by counting pre-retinal nuclei. Retinal pericyte loss was evaluated using retinal trypsin digestion. Electroretinography was performed to examine visual function. No abnormalities were detected in the β-catenin KO mice under normal conditions. In OIR, retinal levels of β-catenin and VEGF were significantly lower in the β-catenin KO mice than in littermate controls. The KO mice also had decreased retinal NV and vascular leakage in the OIR model. In the STZ-induced diabetic model, disruption of β-catenin in Müller cells attenuated over-expression of inflammatory cytokines and ameliorated pericyte dropout in the retina. These findings suggest that Wnt signaling activation in Müller cells contributes to retinal NV, vascular leakage and inflammation and represents a potential therapeutic target for DR.

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Section: Discussionmentioning

confidence: 99%

Interruption of Wnt Signaling in Müller Cells Ameliorates Ischemia-Induced Retinal Neovascularization

Zhou

Benyajati

et al. 2014

PLoS ONE

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“…Variation coefficients are indicated as percent in brackets induced vascular endothelial growth factor (VEGF) local decrease (Alon et al 1995;Claxton and Fruttiger 2003;Gariano and Gardner 2005), which suggests a DEHPcaused delay in maturation of arteriolar wall. So far, quantitative analyses of retinal fluorangiographies have been carried out through the retina partitioning into quadrants and concentric zones, with following count of regions showing lesions of progressive severity (Ricci et al 1990;Penn et al 2001;Zhang et al 2003), or measuring the vascularised and non-vascularised areas (Niesman et al 1997). Thus, to our knowledge, this is the first paper to report the length and area of FITC-dextran perfused retinal vessels.…”

Section: Discussionmentioning

confidence: 99%

DEHP effects on retinal vessels in newborn rats: a qualitative and quantitative analysis

Zei

Pascarella

Barrese

et al. 2009

Histochem Cell Biol

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Di-(2-ethylhexyl)-phthalate (DEHP), employed in polyvinyl chloride fabrication and released by endotracheal tubes, is known to cause alterations to several mammalian tissues, markedly in immature animals. The high incidence and severity of bronchopulmonary dysplasia and retinopathy in preterm babies submitted to endotracheal intubation prompted us to investigate the effects of DEHP in lung and retina perinatal development. We previously demonstrated that in rats delivered and breast-fed by DEHP-treated mothers lung alveolarisation is severely impaired. In the present research, the maturation of retinal vessels was studied in (a) flat-mounted retinas obtained after intracardiac injection of FITC-conjugated dextran, (b) flat-mounted retinas incubated with FITC-conjugated Bandeira simplicifolia isolectin B4, marker of vascular endothelial cells, and (c) eyecup sections incubated with biotinylated IB4 and revealed by ABC. DEHP-induced vascular alterations mainly affected the superficial plexus, where the radial vessels showed non-perfused as well as remarkably dilated and branched segments, capillary net appeared coarsely arranged and locally absent; periarteriolar capillary-free regions were still found in 14-day-old animals. This extensive vascular remodelling and generally the high responsiveness to DEHP shown by the immature rat retina confirm previous hypothesis that the phthalate released by PVC medical devices remarkably affects perinatal development of several tissues in different body districts.

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Section: Discussionmentioning

confidence: 99%

“…Retinopathy of prematurity is a vasoproliferative retinal disease of premature infants. Blindness often results from the aberrant growth of retinal blood vessels and is occasionally associated with fibrous proliferation, retinal detachment or macular ectopia (Ricci et al 1990;Smith et al 1994;Pierce et al 1996). In our current study, using a well-established oxygen-induced ROP model, we investigated whether there were any changes in the expression of GAP 43 and its active form, phospho-GAP 43 and whether pretreatment with TA affected these results.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of triamcinolone acetonide upon the upregulation and phosphorylation of GAP 43 in an animal model of retinopathy of prematurity

Chung

Kim

Park

et al. 2010

Acta Ophthalmologica

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ABSTRACT.Purpose: The aim of the current study was to investigate the effects of triamcinolone acetonide (TA) upon the expression and phosphorylation of growth-associated protein 43 (GAP 43) in the retinas of oxygen-induced retinopathy (OIR) rats.Methods: Oxygen-induced retinopathy was induced by exposing Sprague-Dawley rats to hyperoxia (80% oxygen) from postnatal (P) days 2-14 and then returning the rats to normoxic conditions. Triamcinolone acetonide or a conditioned saline (control) was injected intravitreally into the right or left eye, respectively, of OIR rats at P15. We then assessed the molecular and histological changes in the expression of GAP 43 and phospho-GAP 43 in OIR and control rat retinas, and also after treatment with TA by RT-PCR, Western blotting and immunohistochemistry.Results: Growth-associated protein 43 mRNA levels were found to be increased by 1.6-fold (p = 0.001, n = 5) in the retinas of P18 OIR rats compared with the control rats. The protein levels of GAP 43 and phospho-GAP43 were found to be elevated in the retina of P18 OIR rats (2.40-and 2.39-fold greater than each control, p<0.001, n = 5, respectively). Immunoreactivities of GAP 43 and phospho-GAP 43 were stronger in the inner plexiform layer in OIR rat retinas compared with the control. However, treatment with TA attenuated GAP 43 and phospho-GAP 43 upregulation in the OIR retinas. Conclusion:Our results indicate that GAP 43 and phospho-GAP 43 participate in retinal (potentially pathologic) changes following oxygen-induced damage. Triamcinolone acetonide protects the retinal damage in relatively hypoxic retinas of OIR rats. Therefore, TA treatment does not induce the expression and phosphorylation of GAP 43 in OIR rat retinas.

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Oxygen-induced retinopathy in the newborn rat: a scoring system for the evaluation of retinal vascular changes

Cited by 4 publications

References 14 publications

Interruption of Wnt Signaling in Müller Cells Ameliorates Ischemia-Induced Retinal Neovascularization

Interruption of Wnt Signaling in Müller Cells Ameliorates Ischemia-Induced Retinal Neovascularization

DEHP effects on retinal vessels in newborn rats: a qualitative and quantitative analysis

Protective effects of triamcinolone acetonide upon the upregulation and phosphorylation of GAP 43 in an animal model of retinopathy of prematurity

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