Retinal Angiogenesis in the Human Embryo

Ashton, Norman

doi:10.1093/oxfordjournals.bmb.a070758

Cited by 161 publications

(76 citation statements)

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“…The process of normal vascularization has been extensively examined in the kitten, mouse and rat retinas (Ashton et al, 1957;Ashton, 1961;Ashton, 1970;Blanks and Johnson, 1983;Connolly et al, 1988;Chan-Ling et al, 1990;Smith et al, 1994;Stone et al, 1995;Dorrell and Friedlander, 2006). Several studies have also examined the process in the human fetal retina (Michaelson, 1948;Nilausen, 1958;Cogan, 1963;Ashton, 1970;Nishimura and Taniguchi, 1982;Penfold et al, 1990;Gariano et al, 1994;Hughes et al, 2000).…”

Section: Development Of the Retinal Vasculaturementioning

confidence: 99%

“…Several studies have also examined the process in the human fetal retina (Michaelson, 1948;Nilausen, 1958;Cogan, 1963;Ashton, 1970;Nishimura and Taniguchi, 1982;Penfold et al, 1990;Gariano et al, 1994;Hughes et al, 2000). Development of the retinal vasculature follows a common pattern in all species (Dorrell and Friedlander, 2006), but there are some dissimilarities as well (Ashton, 1968;Gariano et al, 1994).…”

Section: Development Of the Retinal Vasculaturementioning

confidence: 99%

“…Development of the retinal vasculature follows a common pattern in all species (Dorrell and Friedlander, 2006), but there are some dissimilarities as well (Ashton, 1968;Gariano et al, 1994). For example, in humans the process occurs primarily during the latter half of gestation, whereas in rodents the process is completed in the first two weeks after birth (Michaelson et al, 1954;Ashton, 1970;Stone et al, 1995;Engerman and Meyer, 1965). Generally, the completion of retinal vascular development is coincident with eye opening in mammalian species.…”

Section: Development Of the Retinal Vasculaturementioning

confidence: 99%

“…Studies indicate that development of the retinal vasculature may occur by both vasculogenesis, de novo formation of blood vessels from mesodermal precursor cells (angioblasts), and angiogenesis, sprouting of new vessels from existing blood vessels (Ashton, 1966;Ashton, 1970;Flower et al, 1985;McLeod et al, 1987;Kretzer and Hittner, 1988;Chan-Ling et al, 1990;Jiang et al, 1995;Risau and Flamme, 1995;Risau, 1997;Hughes et al, 2000). "Spindle-cells", so called for their shape, have been identified within the inner plexiform layer of the immature mammalian retina (Flower et al, 1985;McLeod et al, 1987;Stone and Dreher, 1987;Watanabe and Raff, 1988;Hughes et al, 2000;Taomoto et al, 2000).…”

Section: 21mentioning

confidence: 99%

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Vascular endothelial growth factor in eye disease

Penn

Madan

Caldwell

et al. 2008

Progress in Retinal and Eye Research

627

527

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Collectively, angiogenic ocular conditions represent the leading cause of irreversible vision loss in developed countries. In the U.S., for example, retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration are the principal causes of blindness in the infant, working age and elderly populations, respectively. Evidence suggests that vascular endothelial growth factor (VEGF), a 40 kDa dimeric glycoprotein, promotes angiogenesis in each of these conditions, making it a highly significant therapeutic target. However, VEGF is pleiotropic, affecting a broad spectrum of endothelial, neuronal and glial behaviors, and confounding the validity of anti-VEGF strategies, particularly under chronic disease conditions. In fact, among other functions VEGF can influence cell proliferation, cell migration, proteolysis, cell survival and vessel permeability in a wide variety of biological contexts. This article will describe the roles played by VEGF in the pathogenesis of retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration. The potential disadvantages of inhibiting VEGF will be discussed, as will the rationales for targeting other VEGF-related modulators of angiogenesis.

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Section: Development Of the Retinal Vasculaturementioning

confidence: 99%

Section: Development Of the Retinal Vasculaturementioning

confidence: 99%

Section: Development Of the Retinal Vasculaturementioning

confidence: 99%

Section: 21mentioning

confidence: 99%

See 2 more Smart Citations

Vascular endothelial growth factor in eye disease

Penn

Madan

Caldwell

et al. 2008

Progress in Retinal and Eye Research

627

527

View full text Add to dashboard Cite

show abstract

“…According to some authors, vascular proliferation never reaches the center of the foveola; others, on the contrary, sustain a later vascular obliteration, regulated by oxygen concentration and by a retinal vas-stimulating factor which becomes inactive at high oxygen concentration (Ashton 1970).…”

Section: Commentmentioning

confidence: 99%

Congenital retinal macrovessels, A "low visual acuity" case report with a 14-year follow-up

Crecchio¹,

Pacente²,

Alfieri³

et al. 1999

Acta Ophthalmologica Scandinavica

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ABSTRACT. We report a rare case of congenital retinal macrovessel with decreased visual acuity, with a 14-year follow-up. Both the clinical findings and the visual acuity remained unchanged throughout the follow-up period.Key words: Congenital retinal macrovessels -decreased visual acuity -retinal fluorangiographycilioretinal artery.Acta Ophthalmol. Scand. 1999; 77: 474-475 Copyright c Acta Ophthalmol Scand 1999. ISSN 1395-3907A 5-year-old child was seen by us in September 1984. Visual acuity was 20/40 in the right eye and 20/20 in the left. Clinical examination yielded nothing remarkable apart from the right fundus, where the presence of an abnormal vein accompanied by a cilioretinal artery was noticed. There were no signs of haemorhages, exudates, aneurysms or edema.Fluorescein angiography (Fig. 1), showed early filling of the anomalous vein, an anomalous capillary network, and slightly delayed emptying of the vein in the right eye. There were no changes in the permeability of the capillary bed.A magnification of the macular area (Fig. 2), is modified to better show the relation between the foveal region and the anomalous vessels. Fluorangiographic study of the left eye showed a normal retina.We performed a complete clinical examination every year for a 14-year follow-up period; the patient was submitted four times to a fluorangiographic examination.No changes were ever noted in the appearance of the right fundus throughout this time (Fig. 3). The visual acuity in the right eye showed no further decrease.The left eye did not present any alteration during the observation period.

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Redistribution and degeneration of retinal astrocytes in experimental murine cerebral malaria: Relationship to disruption of the blood-retinal barrier

Medana

Chan‐Ling

Hunt

1996

Glia

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To determine whether astrocytes play a critical role in the pathogenesis of experimental murine cerebral malaria (EMCM), we examined changes in astrocyte morphology and distribution, using retinal wholemounts, in three models: a fatal cerebral malaria (CM) model, in which mice die showing cerebral symptoms; a “resolving” model, in which mice exhibit mild cerebral symptoms, but then recover; and a non‐CM model, in which cerebral symptoms are not seen. In the fatal model, retinal astrocytes lost their even distribution from day 3 post‐inoculation (p.i.) with malaria parasites, progressing to gliosis (day 5 p.i.), well before the onset of cerebral symptoms on day 6–7 p.i. At the terminal stage of the disease there was a loss of astrocyte processes contacting retinal vessels, often along vessel segments containing adherent monocytes. These features occurred in a mild form in the resolving model and were absent in the non‐CM models. To investigate the mechanisms underlying these astrocytic changes, we carried out two experimental manipulations. Firstly, since dexamethasone ameliorates cerebral complications in the fatal CM model, the astrocytic response was monitored after dexamethasone treatment on days 0 and 1 p.i., or days 3 and 4 p.i. Second, to determine whether increased blood‐retinal barrier (BRB) permeability initiates the astrocyte changes, breakdown of the BRB was induced experimentally by intra‐carotid injection of arabinose and astrocyte morphology and distribution were examined 12, 24, and 48 h later. Retinal astrocytes in both the dexamethasone‐ and the arabinose‐treated groups showed loss of even astrocyte distribution but no loss of astrocyte ensheathment of vessels. It is concluded that: i) astrocytes are involved in the pathogenesis of EMCM, since these changes are only prominent in the fatal model and occur substantially before the onset of cerebral symptoms; ii) the initial changes in astrocyte distribution may be a consequence of the increase in BRB permeability; and iii) the immune response triggered by the malaria parasite may be responsible for the loss of astrocyte ensheathment of vessel segments. © 1996 Wiley‐Liss, Inc.

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Retinal Angiogenesis in the Human Embryo

Cited by 161 publications

References 0 publications

Vascular endothelial growth factor in eye disease

Vascular endothelial growth factor in eye disease

Congenital retinal macrovessels, A "low visual acuity" case report with a 14-year follow-up

Redistribution and degeneration of retinal astrocytes in experimental murine cerebral malaria: Relationship to disruption of the blood-retinal barrier

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