Advanced Glycation End Products Induce Expression of Vascular Endothelial Growth Factor by Retinal Müller Cells.

Hirata, Chiaki; Nakano, Kayo; Nakamura, Nobutaka; Kitagawa, Yasuhide; Shigeta, Hirofumi; Hasegawa, Go; Ogata, Masafumi; Ikeda, Tomohiro; Sawa, Hirofumi; Nakamura, Kayo; Ienaga, Kazuharu; Obayashi, Hiroshi; Kondo, Megumi

doi:10.1097/00006982-199805000-00029

Cited by 25 publications

(32 citation statements)

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“…However, corneal AGE fluorescence values increased only in the patients with PDR. The vitreous concentrations of AGEs and vascular endothelial growth factor (VEGF) were both elevated in the patients with PDR (5, 17,18). VEGF plays a role in breakdown of the blood-retinal barrier (BRB) (19 -21).…”

Section: Discussionmentioning

confidence: 99%

Corneal Advanced Glycation End Products Increase in Patients With Proliferative Diabetic Retinopathy

et al. 2001

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OBJECTIVE—To evaluate corneal advanced glycation end product (AGE) fluorescence in patients with diabetes and in healthy control subjects. RESEARCH DESIGN AND METHODS—Corneal autofluorescence was measured in 26 eyes of 26 patients with type 2 diabetes (mean age 57.0 years; mean disease duration 12.2 years; mean HbA1c 7.1%) and 13 eyes of 13 healthy age-matched control subjects (mean age 57.9 years). The patients with type 2 diabetes were divided into the following groups: patients without diabetic retinopathy (DR), patients without proliferative diabetic retinopathy (PDR), and patients with PDR. Corneal autofluorescence was measured by fluorophotometry with the wavelength that is characteristic of AGE fluorescence (excitation and emission 360–370 nm and 430–450 nm, respectively). We defined peak corneal autofluorescence levels as corneal AGE fluorescence values. We compared the corneal AGE fluorescence values in the four groups. RESULTS—In the PDR group (11.9 ± 3.9 arbitrary units [mean ± SD]), the corneal AGE fluorescence values were significantly higher compared with the control subjects (6.9 ± 1.3 arbitrary units), the patients without DR (7.4 ± 2.1 arbitrary units), and the patients without PDR (6.9 ± 2.2 arbitrary units) (P < 0.05). CONCLUSIONS—We found that corneal AGEs may increase in patients with diabetes and PDR compared with control subjects, patients without DR, and patients without PDR. In the patients with PDR, increased corneal AGEs may play a role in diabetic keratopathy.

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Section: Discussionmentioning

confidence: 99%

Corneal Advanced Glycation End Products Increase in Patients With Proliferative Diabetic Retinopathy

et al. 2001

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“…Serum concentrations of soluble tumor necrosis factor-alpha receptor I (sTNFRI), IL-6, VEGF, MRP 8/MRP 14, S100A12, and soluble receptor for advanced glycation end product (sRAGE) were determined by a sandwich enzyme-linked immunosorbent assay (ELISA). Commercial kits to quantitative human sTNFRI (Bender MedSystem, Vienna, Austria), human IL-6 (BioSource International, CA), human VEGF (Immuno-Biologic Laboratories, Fujioka, Japan), and sRAGE (Quantikine; R&D Systems, Minneapolis, MN) were used according to the manufacturer-recommended procedures (17,18). Serum concentrations of S100A12 and MRP8/MRP14 were determined by a double-sandwich ELISA using a specific antibody without cross reactivity to other S100 proteins, as described previously (19).…”

Section: Methodsmentioning

confidence: 99%

Infliximab Reduces the Cytokine-Mediated Inflammation but Does Not Suppress Cellular Infiltration of the Vessel Wall in Refractory Kawasaki Disease

et al. 2009

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ABSTRACT:The aim of our study was to evaluate the efficacy of infliximab for the treatment of patients with refractory Kawasaki disease (KD) and investigate the dynamic changes of cytokines during infliximab treatment. We have performed a study of cytokine and proinflammatory molecule levels in 43 KD patients including 18 responders to IVIG, 14 nonresponders, and 11 patients treated with infliximab. We determined serum levels of soluble TNF receptor I (sTNFR I) and IL-6, as well as VEGF, damage associated molecular pattern (DAMP) molecules; myeloid-related protein (MRP)8/MRP14 and S100A12 sequentially. In eight patients, fever subsided immediately upon infliximab treatment. Four patients, who started infliximab after 12 d of illness, developed coronary artery lesions. Each of the cytokines was elevated before infliximab treatment in all patients. Although serum levels of proinflammatory cytokines decreased dramatically after infliximab treatment, DAMP molecules and VEGF and markers of local tissue damage were not suppressed. In contrast, in IVIG responders all cytokines decreased markedly after IVIG treatment. We show that infliximab is one of the adoptive therapies in refractory KD patients. Different behaviors of proinflammatory cytokines and DAMP molecules and VEGF after infliximab treatment suggest that infliximab is effective for suppression of cytokinemediated inflammation, but could not completely block local vasculitis. (Pediatr Res 65: 696-701, 2009) K awasaki disease (KD) is the most common systemic vasculitis syndrome primarily affecting small and medium-sized arteries, particularly the coronary artery. Although timely treatment with high-dose i.v. immune globulin (IVIG) is now accepted as reducing the incidence of coronary artery lesions (CAL), approximately 15% of the patients do not respond to IVIG treatment and have persistent fever as a manifestation of ongoing inflammation. These patients are at highest risk for development of CAL (1). The current practice for patients with KD and persistent or recrudescent fever after IVIG is to institute additional therapies, which may include one or more repeat doses of IVIG, high-dose pulse methylprednisoline, cyclophosphamide, methotrexate, ulinastatin, cyclosporine A (CyA), or plasmapheresis (2,3). Recently, potential new therapeutic approaches with infliximab (Remicade), a chimeric mouse-human MAb against tumor necrosis factor (TNF)-␣, have been reported in refractory KD patients (4).During the acute phase of KD, serum levels of proinflammatory cytokines such as TNF-␣ are elevated (5). In experimental studies of this syndrome, characterized by vasculitis resulting in coronary, as well as extracoronary, aneurysms, and stenosis, the attenuation of cytokine responses, especially IL-6, after infusions of IVIG may play an integral role in the rapid resolution of most of the symptoms in children with KD (6). In addition to these proinflammatory cytokines, VEGF, and markers of local inflammation of the family of damageassociated molecular pattern molecules (DAMP...

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“…80, No. 8, p. 1171 Copyright © 2000 of this cytokine appears be stimulated by local ischemia (Armstrong et al, 1998) or by general factors such as high concentrations of glucose (Natarajan et al, 1997) and advanced glycation end products (Hirata et al, 1997). The question addressed in this paper is whether vascular beds other than those generally known to be affected by diabetes (eye, kidney, and nerves) are also susceptible to alteration by this disease.…”

mentioning

confidence: 94%

“…This abnormal endothelial proliferation is at present explained by the expression, at the affected site, of endothelial growth factors, particularly the vascular endothelial growth factor (VEGF). Synthesis of this cytokine appears be stimulated by local ischemia (Armstrong et al, 1998) or by general factors such as high concentrations of glucose (Natarajan et al, 1997) and advanced glycation end products (Hirata et al, 1997).…”

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confidence: 99%

Alterations of the Rat Mesentery Vasculature in Experimental Diabetes

Arshi

Bendayan

Ghitescu

2000

Laboratory Investigation

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SUMMARY:The alteration induced by diabetes on vascular permeability to serum albumin was investigated in the mesentery of streptozotocin-induced hyperglycemic rats. Double-tagged ( 125 I and dinitrophenol-haptenated) heterologous albumin was intravenously administered in normal and hyperglycemic animals, and the extravasation of the tracer was evaluated by radioactivity measurements and by morphometry at the ultrastructural level using quantitative protein A-colloidal gold immunocytochemistry. The results demonstrate that diabetes induces a significant increase in the permeability of the mesentery vessels to albumin. This increase is due to a more efficient transport of macromolecules by endothelial plasmalemmal vesicles and not to leakier interendothelial junctions. Passage across the endothelial basement membranes did not appear to be restricted in either the control or diabetic condition. However, in diabetes, the mesothelial basement membrane appeared to become modified and to restrain the passage of albumin toward the peritoneal cavity. After 3 months of diabetes, the rats presented a net increase in the average diameter of the blood vessels localized in the mesentery arcada (macrovascular hyperplasy) and a notable angiogenesis, manifested at the level of the microvasculature in the mesenteric windows. (Lab Invest 2000, 80:1171-1184.T he association of diabetes with vascular dysfunctions gradually evolving toward incapacitating or life-threatening vascular pathologies is undisputed. Extensive clinical observations and studies on animal models have amply documented that hyperglycemia accelerates and worsens atherosclerosis in large arteries (Colwell et al, 1988;Shantaram, 1999;Steiner 1997) and affects, although in different ways, the microvessels of selected vascular beds, such as those of the retina (Bazan et al, 1997;Cunha-Vaz, 1983;Porta, 1996;Ruggiero et al, 1997), kidney (Flyvbjerg, 1997;Mauer et al, 1984;Nyengaard and Bendtsen, 1993;Vlassara et al, 1994), and nerves (Cameron and Cotter, 1997;Malik et al, 1993; Tesfay et al, 1994). Particular attention has been directed to the study of diabetes-induced retinopathies and nephropathies, because of their obvious clinical implications. On the other hand, the impact of diabetes on other vascular beds has been generally overlooked. Therefore, it is not known whether diabetic microangiopathy concerns all blood vessels, creating a sort of "dysfunctional background" exacerbated in particular tissues by local factors to a full blown vascular pathology, or the vasculature of many organs is simply spared by the deleterious effects of hyperglycemia/ hypoinsulinemia. The latter hypothesis would fall in line with the ever-growing body of evidence pointing to important physiological and biochemical dissimilarities between various vascular segments (Boegehold, 1998;Rajotte et al, 1998;Thorin and Shreeve, 1998).Several morphologic features and physiologic parameters appear as leit motifs of diabetic microangiopathies. Among these, the thickening of the basement membran...

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Advanced Glycation End Products Induce Expression of Vascular Endothelial Growth Factor by Retinal Müller Cells.

Cited by 25 publications

References 0 publications

Corneal Advanced Glycation End Products Increase in Patients With Proliferative Diabetic Retinopathy

Corneal Advanced Glycation End Products Increase in Patients With Proliferative Diabetic Retinopathy

Infliximab Reduces the Cytokine-Mediated Inflammation but Does Not Suppress Cellular Infiltration of the Vessel Wall in Refractory Kawasaki Disease

Alterations of the Rat Mesentery Vasculature in Experimental Diabetes

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