Prevention of Pericyte Ghost Formation in Retinal Capillaries of Galactose-Fed Dogs by Aldose Reductase Inhibitors

Kador, Peter F.; Akagi, Yoshio; Terubayashi, H; Wyman, Milton; Kinoshita, Jin H.

doi:10.1001/archopht.1988.01060140255036

Cited by 106 publications

(41 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Nevertheless, the association among hyperglycemia, diabetes, and retinopathy remains to be mechanistically defined (Addison et al, 1970;Harik and LaManna, 1988;Kern and Engerman, 1996;Mann et al, 2003). The primary mechanisms implicated in the pathogenesis of diabetic retinopathy are thought to be biochemical and hemodynamic, all of which are dependent on excessive transport (GLUT-1) or accumulation of glucose (Kumagai, 1999;Lorenzi et al, 1986) within the retina or its microvasculature (Kador et al, 1988;Kern and Engerman, 1986;Mizutani et al, 1996). The results of this study reveal that the increased retinal glucose levels in the group of diabetic rats are not a consequence of increased glucose crossing the BRB.…”

Section: Discussionsupporting

confidence: 38%

Comparison of Glucose Influx and Blood Flow in Retina and Brain of Diabetic Rats

Puchowicz

Magness

et al. 2004

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Summary:Diabetes is associated with extensive microvascular pathology and decreased expression of the glucose transporter (GLUT-1) in retina, but not brain. To explore the basis of these differences, the authors simultaneously measured glucose influx (mol · g −1 · min) and blood flow (mL · g −1 · min −1 ) in retina and brain cortex of nondiabetic control rats (normoglycemic and acute-hyperglycemic) and in rats with streptozotocin-induced diabetes (with or without aminoguanidine (AMG) treatment) using a single-pass, dual-label indicator method. In addition, tissue glucose and adenosine triphosphate (nmol/mg dry weight) levels were measured. Glucose influx in retina exceeded that of cortex by about threefold for both the nondiabetic and diabetic groups. In contrast, blood flow in retina was significantly lower than in cortex by about threefold for each group. Retinal and cortical glucose influx in the diabetic rats was lower than in the nondiabetic acute-hyperglycemic group, but not in the normoglycemic group. Blood flow in these tissues remained relatively unchanged with glycemic conditions. The glucose levels in the diabetic retina (aminoguanidine untreated and aminoguanidine treated) were fourfold to sixfold greater than the nondiabetic retina. The cortical glucose levels remained unchanged in all groups. These data suggest that the accumulation of glucose in the diabetic retina cannot be explained by increased endothelialglucose uptake or increased vascular membrane permeability.

show abstract

Section: Discussionsupporting

confidence: 38%

Comparison of Glucose Influx and Blood Flow in Retina and Brain of Diabetic Rats

Puchowicz

Magness

et al. 2004

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

show abstract

“…In addition to cataract formation, long term galactose-feeding induces retinal vessel changes in dogs (Engerman and Kern, 1984 ;Kador et al, 1988 ;Takahashi et al, 1992 ;Kador et al, 1995). When 9-month old dogs are fed galactose, retinal capillary pericyte degeneration with development of pericyte ghosts occurs after 19 months of galactose feeding (Kador et al, 1990).…”

Section: Discussioncontrasting

confidence: 38%

“…To address the importance of aldose reductase in initiating sugar cataract formation in the dog, prevention studies using 10 and 16 mg kg −" of the aldose reductase inhibitor M79175 have been conducted to determined whether dose-dependent inhibition of cataract formation can be demonstrated. (Kador et al, 1988 ;1994). M79175 (2-methyl-6-fluorospirochroman-4-5h-imidazolidine2h,4h-dione) administered in capsules were a gift from the Eisai Pharmaceutical Co., Tokyo, Japan.…”

Section: Introductionmentioning

confidence: 43%

Dose-Dependent Prevention of Sugar Cataracts in Galactose-fed Dogs by the Aldose Reductase Inhibitor M79175

Sato

Mori

Wyman

et al. 1998

Experimental Eye Research

View full text Add to dashboard Cite

“…The pathogenesis of the pericyte damage is incompletely understood, although it is likely to be the consequence of altered glucose metabolism, leading to polyol accumulation [Kador et al, 1988;Hohman et al, 1989] or an increase in toxic advanced glycation end products [Chibber et al, 1997]. The precise link between the loss of pericytes and the lesions seen in diabetic retinopathy is not yet known, although it is notable that microaneurysms occur where there is an absence of pericytes [Cogan et al, 1961;Robison et al, 1990Robison et al, , 1991.…”

Section: Pathologysupporting

confidence: 41%

Pericytes: Cell Biology and Pathology

Allt

Lawrenson

2001

Cells Tissues Organs

406

298

View full text Add to dashboard Cite

Pericytes are perivascular cells with multifunctional activities which are now being elucidated. The functional interaction of pericytes with endothelial cells (EC) is now being established, using current molecular and cytochemical techniques. The detailed morphology of the pericyte has been well described. Pericytes extend long cytoplasmic processes over the surface of the EC, the two cells making interdigitating contacts. At points of contact, communicating gap junctions, tight junctions and adhesion plaques are present. Pericytes appear to show both structural and functional heterogeneity. The coverage of EC by pericytes varies considerably between different microvessel types and the location of pericytes on the microvessel is not random but appears to be functionally determined. Interaction between pericytes and EC is important for the maturation, remodelling and maintenance of the vascular system via the secretion of growth factors or modulation of the extracellular matrix. There is also evidence that pericytes are involved in the transport across the blood-brain barrier and the regulation of vascular permeability. The long-standing view that pericytes are the microvessel equivalent of larger vessel smooth muscle cells and are contractile is being reassessed using current methods. An important role for pericytes in pathology, and neuropathology in particular, has been indicated in hypertension, diabetic retinopathy, Alzheimer’s disease, multiple sclerosis and CNS tumour formation.

show abstract

Prevention of Pericyte Ghost Formation in Retinal Capillaries of Galactose-Fed Dogs by Aldose Reductase Inhibitors

Cited by 106 publications

References 6 publications

Comparison of Glucose Influx and Blood Flow in Retina and Brain of Diabetic Rats

Comparison of Glucose Influx and Blood Flow in Retina and Brain of Diabetic Rats

Dose-Dependent Prevention of Sugar Cataracts in Galactose-fed Dogs by the Aldose Reductase Inhibitor M79175

Pericytes: Cell Biology and Pathology

Contact Info

Product

Resources

About