Demonstration of vasoproliferative activity from mammalian retina.

Glaser, Bert M.; D’Amore, Patricia A.; Michels, Ronald G.; Patz, Arnall; Fenselau, Allan

doi:10.1083/jcb.84.2.298

Cited by 260 publications

(78 citation statements)

References 15 publications

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“…There are present in the retina of both kittens (16,17) and humans (1 8) potent growth factors that stimulate endothelial proliferation, migration, and angiogenesis. It would be consistent for oxygen to play an important role in affecting the release of (13), the tapered group were slowly withdrawn from oxygen over 3.5 wk (14), and the variable kittens were recovered in an incubator cycling between 8 and 43%, oxygen (14).…”

Section: Resultsmentioning

confidence: 99%

Reduced Severity of Oxygen-Induced Retinopathy in Kittens Recovered in 28% Oxygen

Phelps

1988

Pediatr Res

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ABSTRACT. Chronic hypoxemia adversely affects the retinopathy observed in kittens after a hyperoxic exposure (80% oxygen) in the 1st wk of life. To test the converse hypothesis, 55 kittens were randomly assigned to recover in room air (21%) or 28% inspired oxygen after a 65-h hyperoxic exposure. At 4 wk of age, the retinopathy was found to be less severe in the 28% recovered kittens, severity score 3.0 f 3.3 (mean -+ SD), than in the room air recovered animals, severity score 5.7 f 3.3, p < 0.01. This finding suggests that the clinical practice of restricted oxygenation in premature infants warrants reevaluation. (Pediatr Res 24: 106-109, 1988) Abbreviation ROP, retinopathy of prematurity ROP has been linked with supplemental oxygen administration since the 1950s when it was determined that the prolonged (more than 4 wk) use of more than 50% inspired oxygen in human premature infants without regard to cyanosis caused a 10-fold increase in severe ROP (1). Animal models of this disorder further reinforced the association with oxygen because a similar retinopathy can be produced in kittens, puppies, mice, and some other mammals by exposing them to high inspired oxygen during the 1st wk of life (2-4). This oxygen-induced retinopathy, however, does not progress to full retinal detachment and blindness, as ROP does in some infants. However, major clinical and research efforts have been aimed at preventing vision loss in infants through ever tightening control of oxygen administration (5, 6). Despite this, the disorder remains a significant problem in the 1980s, even with the most stringent oxygen monitoring efforts (7).While immaturity of the retinal vasculature at the time of birth is clearly the dominant determinant of risk for ROP, case control studies have found that the degree of illness and number of complications after delivery significantly affect the risk of severe disease after adjusting for the infant's level of immaturity (8-12). The observation that among the most premature infants, Received December 15, 1987; accepted March 15, 1988 the sickest and most unstable are at greater risk for vision loss than those whose clinical course goes smoothly led to the investigation of variable oxygenation after a retinal vascular injury. The sickest infants have more unstable oxygenation status, and on average lower arterial oxygen levels than stable infants (10). Therefore the effects of chronic hypoxia and extremely variable oxygenation were studied in the kitten model of oxygen-induced retinopathy. In this model, an initial injury to the retinal vasculature was caused by exposing the kittens to 80% oxygen for 65 h followed by a 3-wk recovery period. Quite clearly, hypoxia during the recovery period adversely affected the retinopathy (1 3), but surprisingly, a variable oxygenation status appeared to reduce its severity (14). In reporting the results of that study, we speculated that the wide but rapid (18 min) swings of oxygen from 8 to 43% where experienced by the retina as a single average effect. By integrating ...

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Section: Resultsmentioning

confidence: 99%

Reduced Severity of Oxygen-Induced Retinopathy in Kittens Recovered in 28% Oxygen

Phelps

1988

Pediatr Res

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“…In vivo angiogenesis assays have shown that bFGF is a very potent angiogenic factor (Glaser et al, 1980a(Glaser et al, , 1980bWong et al, 2001). It is also increased in vitreous samples from patients with PDR (Sivalingam et al, 1990).…”

Section: Basic Fibroblast Growth Factor (Bfgf)mentioning

confidence: 99%

Growth Factors in Proliferative Diabetic Retinopathy

Khan

Chakrabarti

2003

Journal of Diabetes Research

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Many growth factors are implicated in the pathogenesis of proliferative diabetic retinopathy. Alteration of growth factors and their receptors in diabetes has been shown in both experimental and clinical studies. Sustained hyperglycemia resulting from long-standing diabetes leads to several biochemical abnormalities that consequently result in retinal hypoxia. Retinal oxygenation state regulates various growth factors that promote angiogenesis in order to meet the oxygen demands of the tissue. However, unregulated expression of these growth factors and induction of complex cascades leading to augmentation of other proangiogenic factors, which may not be regulated by tissue oxygenation, leads to uncontrolled retinal neovascularization and blindness in diabetic patients.

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“…Basal culture medium was alpha minimal essential medium (GIBCO, Grand Island, N.Y.) with 20% heat-inactivated fetal bovine serum (HyClone Laboratories, Logan, Utah), 100 g of heparin (Sigma) per ml, 50 U of penicillin per ml, and 50 g of streptomycin per ml (defined as complete medium [CM]). HUVEC were suspended at a concentration of 10 3 /ml in CM supplemented with 10 l of bovine retinal extract per ml (CM-BRE) prepared as described previously (7,29). HUVEC were seeded in culture dishes (6-cm diameter; Falcon; Becton Dickinson Labware, Oxnard, Calif.) coated with human fibronectin (1 g/cm 2 ) and incubated at 37°C in humidified 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

Pathogenic Mechanism of Mouse Brain Damage Caused by Oral Infection with Shiga Toxin-ProducingEscherichia coliO157:H7

Kita¹,

Yunou²,

Kurioka³

et al. 2000

Infect Immun

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In a previous study, we showed that infection with Shiga toxin (Stx)-producing Escherichia coli O157:H7 (strain Sm r N-9) caused neurologic symptoms in malnourished mice with positive immunoreactions of Stx2 in brain tissues. The present study explores the mechanism of how Stx injures the vascular endothelium to enter the central nervous system in mice. Oral infection with strain Sm r N-9 elicited a tumor necrosis factor alpha (TNF-␣) response in the blood as early as 2 days after infection, while Stx was first detected at 3 days postinfection. In the brain, TNF-␣ was detected at day 3, and its quantity was increased over the next 3 days. Frozen sections of the brains from moribound mice contained high numbers of apoptotic cells. Glycolipids recognized by an anti-Gb3 monoclonal antibody were extracted from the brain, and purified Stx2 was able to bind to the glycolipids. In human umbilical vascular endothelial cells (HUVEC) cultured with fluorescein-labeled Stx2 (100 ng/ml), TNF-␣ (20 U/ml) significantly facilitated the intracellular compartmentalization of fluorescence during 24 h of incubation, suggesting the enhanced intracellular processing of Stx2. Consequently, higher levels of apoptosis in HUVEC were found at 48 h. Short-term exposure of HUVEC to Stx2 abrogated their apoptotic response to subsequent incubation with TNF-␣ alone or TNF-␣ and Stx2. In contrast, primary exposure of HUVEC to TNF-␣ followed by exposure to Stx2 alone or TNF-␣ and Stx2 induced apoptosis at the same level as obtained after 48-h incubation with these two agents. These results suggest that the rapid production of circulating TNF-␣ after infection induces a state of competence in vascular endothelial cells to undergo apoptosis, which would be finally achieved by subsequent elevation of Stx in the blood. In this synergistic action, target cells must be first exposed to TNF-␣. Such cell injury may be a prerequisite to brain damage after infection with Stx-producing E. coli O157:H7.

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Demonstration of vasoproliferative activity from mammalian retina.

Cited by 260 publications

References 15 publications

Reduced Severity of Oxygen-Induced Retinopathy in Kittens Recovered in 28% Oxygen

Reduced Severity of Oxygen-Induced Retinopathy in Kittens Recovered in 28% Oxygen

Growth Factors in Proliferative Diabetic Retinopathy

Pathogenic Mechanism of Mouse Brain Damage Caused by Oral Infection with Shiga Toxin-ProducingEscherichia coliO157:H7

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