Pericytes in diabetic retinopathy.

Oliveira, F. de

doi:10.1136/bjo.50.3.134

Cited by 110 publications

(37 citation statements)

References 11 publications

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“…This is in contrast to reports on retinopathy in KKmice where a decreased frequency of mural cells has been reported (Duhault et al 1973(Duhault et al , 1974. Also in retinopathy in rats (Leuenberger et al 1971(Leuenberger et al , 1974Cohen et al 1972) and in humans (Cogan et al 1961;;Kuwabara & Cogan 1963a;de Oliveira 1966;Yanoff 1972) disappearance of mural cells has been noted. U p till now there has been no evidence, however, that the mural cells are of significance in the aetiology of diabetic retinopathy (Cogan et al 1967;Yanoff 1969).…”

Section: Retinal Cafillaries In Obese-hyperglycemic Micecontrasting

confidence: 80%

Morphology and Enzyme Activities of the Retinal Capillaries in Mice With the Obese‐hyperglycaemic Syndrome (Gene Symbol Ob)

Naeser

Ågren

1978

Acta Ophthalmologica

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The retinal capillary bed from 67 obese-hyperglycaemic mice and 64 lean litter mates was isolated by trypsin digestion and investigated with respect to structure and enzyme activities. There was no significant difference in the ratio between numbers of endothelial and mural cells. The capillary walls did not show any obvious structural differences and microaneurysms were not observed. The retinal vessels from the obese-hyperglycaemic mice, however, displayed significantly higher activities of the enzymes hydroxyacyl-CoA-dehydrogenase, asparate aminotransferase (ASAT) and adenylate kinase than their lean litter mates. The activities of glutathione reductase, glucose-6-phosphate dehydrogenase (G-6-PDH) and phosphofructokinase were similar in the two experimental groups. It is suggested that the present data reflect early metabolic disturbances related to diabetic retinopathy.

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Section: Retinal Cafillaries In Obese-hyperglycemic Micecontrasting

confidence: 80%

Morphology and Enzyme Activities of the Retinal Capillaries in Mice With the Obese‐hyperglycaemic Syndrome (Gene Symbol Ob)

Naeser

Ågren

1978

Acta Ophthalmologica

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“…Proliferative retinopathy is present in 25% of patients with type 1 diabetes after 15 years of diabetes duration and in >50% after 20 years (25). Loss of retinal pericytes together with basement membrane thickening represents early signs of diabetic retinopathy, and pericyte loss has been considered to be the primary lesion in the development of retinopathy (13).…”

Section: Introductionmentioning

confidence: 99%

Bovine Retinal Pericytes Are Resistant to Glucose-Induced Oxidative StressIn Vitro

Agardh

Hultberg

Nayak

et al. 2005

Antioxidants & Redox Signaling

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Diabetic retinopathy is a sight-threatening complication of diabetes, and loss of pericytes represents early signs of its development. We tested the hypothesis that high glucose levels may induce signs of oxidative stress in cultured bovine retinal pericytes. Pericytes were exposed to either normal (5.5 mM) or high (22 mM) glucose levels for 1, 3, and 5 days. Signs of oxidative stress were measured by expression of copper/zinc superoxide dismutase, manganese superoxide dismutase, catalase, and glutathione peroxidase using real-time RTPCR. To elucidate the role of oxidative stress, we also measured glutathione (GSH) concentration in the cells and investigated the impact of thiol-reactive metal ions and hydrogen peroxide (H(2)O(2)) on intracellular GSH. Despite the stimulation with high glucose, thiol-reactive metal ions, or H(2)O(2), there was no clear increased expression of antioxidant enzymes or influence of GSH levels. Lipid peroxidation (malondialdehyde level) was increased in bovine aortic smooth muscle cells, but not in bovine retinal pericytes. The data indicate that pericytes do not develop oxidative stress in response to hyperglycemia. However, it is not definitively excluded that oxidative stress may occur after longer time periods of glucose stimulation.

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“…Retina and cerebral cortex are embryologically similar, yet, we and others (9)(10)(11) have found them to differ in their susceptibility to develop microvascular lesions of diabetes. Unlike the extensive microvascular pathology that develops in retinal capillaries in diabetes, cerebral capillaries show no increase in the number of acellular capillaries, microaneurysms, or pericyte ghosts (11).…”

mentioning

confidence: 99%

Diabetes downregulates GLUT1 expression in the retina and its microvessels but not in the cerebral cortex or its microvessels.

et al. 2000

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Capillaries in the retina are more susceptible to develop microvascular lesions in diabetes than capillaries in the embryologically similar cerebral cortex. Because available evidence implicates hyperglycemia in the pathogenesis of diabetic retinopathy, differences in glucose transport into the retina and brain might contribute to this observed tissue difference in susceptibility to diabetes-induced microvascular disease. Thus, we compared levels of GLUT1 and GLUT3 expression in the retina, cerebrum, and their respective microvessels by Western blot analysis. In nondiabetic animals, the content of GLUT1 protein in retina and its microvessels was multifold greater than that of cerebral cortex gray matter and its microvessels. Streptozotocin-induced diabetes of a 2-week or 2-month duration reduced GLUT1 expression in the retina and its microvasculature bỹ 50%, but it resulted in no reduction in GLUT1 expression in cerebrum or its microvessels. The density of capillaries in retinas of diabetic animals did not change from normal, and so the observed decrease in GLUT1 expression in the retina and retinal capillaries of diabetic animals cannot be attributed to fewer vessels. Despite the diabetes-induced reduction of GLUT1 expression in retina, neural retina of diabetic rats still possessed more GLUT1 than the cerebrum. Retinal pigment epithelium (RPE) possessed more GLUT1 than neural retina or its microvessels, and expression of the transporter in the RPE was not affected by diabetes. GLUT3 levels were greater in cerebral gray matter than in retina, and they were unaffected by diabetes in either tissue. The effect of diabetes on GLUT1 expression differs between retina and cerebral cortex, suggesting that glucose transport is regulated differently in these embryologically similar tissues. Because diabetes results in downregulation of GLUT1 expression in retinal microvessels, but not in RPE, the fraction of the glucose entering the retina in diabetes is likely to be greater across the RPE than across the retinal vasculature. Diabetes 49:1016-1021, 2000 H yperglycemia is sufficient to initiate the development of diabetic retinopathy. This fact has been made especially clear by the development of diabetic-like retinopathy in normal nondiabetic dogs and rodents that were experimentally made hyperglycemic by feeding them a diet enriched with galactose (1-5). Studies demonstrating that intensive therapy sufficient to minimize hyperglycemia inhibits the development of retinopathy (6-8) are consistent with the evidence that hyperglycemia plays a critical role in the pathogenesis of retinal disease. However, the mechanism by which hyperglycemia causes diabetic retinopathy remains unclear. Excessive transport or concentration of glucose within cells of the retina is a common thread underlying most of the biochemical mechanisms that have been postulated to play a role in the pathogenesis of diabetic retinopathy.Retina and cerebral cortex are embryologically similar, yet, we and others (9-11) have found them to differ in their sus...

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Pericytes in diabetic retinopathy.

Cited by 110 publications

References 11 publications

Morphology and Enzyme Activities of the Retinal Capillaries in Mice With the Obese‐hyperglycaemic Syndrome (Gene Symbol Ob)

Morphology and Enzyme Activities of the Retinal Capillaries in Mice With the Obese‐hyperglycaemic Syndrome (Gene Symbol Ob)

Bovine Retinal Pericytes Are Resistant to Glucose-Induced Oxidative StressIn Vitro

Diabetes downregulates GLUT1 expression in the retina and its microvessels but not in the cerebral cortex or its microvessels.

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