Vascular Endothelial Growth Factor in Ocular Fluid of Patients with Diabetic Retinopathy and Other Retinal Disorders

Aiello, L P; Rl, Avery; Pg, Arrigg; Ba, Keyt; Hd, Jampel; St, Shah; Lr, Pasquale; Thieme, Hagen; Ma, Iwamoto; Park, Je

doi:10.1056/nejm199412013312203

Cited by 3,388 publications

(1,843 citation statements)

References 28 publications

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“…RT-PCR and Western blot analysis indicated that VEGF-B was expressed by seven of seven CRC cell lines utilized in this study (not shown), suggesting that VEGF ligands may be involved in an autocrine loop activating VEGFR-1. PlGF, which also acts as a ligand for VEGFR-1 (Aiello et al, 1994), was also expressed by two of seven of the CRC cell lines tested (RT-PCR data not shown) and hence may be implicated as well. Although our studies demonstrate a role for VEGFR-1 in steps involved in tumor progression and metastasis, it is unknown what role neuropilin-1 (NRP-1) plays in modifying these effects.…”

Section: Discussionmentioning

confidence: 99%

Expression and function of vascular endothelial growth factor receptor-1 on human colorectal cancer cells

et al. 2005

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Section: Discussionmentioning

confidence: 99%

Expression and function of vascular endothelial growth factor receptor-1 on human colorectal cancer cells

et al. 2005

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“…Wautier et al (44) reported that infusion of diabetic red blood cells into normal rats can induce vascular hyperpermeability, which was completely inhibited by anti-RAGE IgG; they also demonstrated that an antioxidant, probucol, can similarly reverse the red blood cell transfer-induced vascular permeability, suggesting a role of AGE-RAGE interactions and the involvement of an oxidant stress-sensitive pathway in the development of hyperpermeability. Recent clinical studies at different institutions have established that intraocular concentrations of VEGF correlated with active neovascularization (45,46). Further, the increased permeability of retinal capillaries and the breakdown of the blood-retinal barrier have been shown to be as an early event in both human diabetic subjects and streptozotocin diabetic rats followed by new vessel formation (47,48).…”

Section: Discussionmentioning

confidence: 99%

Advanced Glycation End Products-driven Angiogenesis in Vitro

Yamagishi

Yonekura

Yamamoto

et al. 1997

Journal of Biological Chemistry

260

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This study was undertaken to determine whether and how advanced glycation end products (AGE), senescent macroproteins accumulated in various tissues under hyperglycemic states, cause angiogenesis, the principal vascular derangement in diabetic microangiopathy. We first prepared AGE-bovine serum albumin (BSA) and anti-AGE antiserum using AGE-RNase A. Then AGE-BSA was administered to human skin microvascular endothelial cells in culture, and their growth was examined. The AGE-BSA, but not nonglycated BSA, was found to induce a statistically significant increase in the number of viable endothelial cells as well as their synthesis of DNA. The increase in DNA synthesis by AGE-BSA was abolished by anti-AGE antibodies. AGE-BSA also stimulated the tube formation of endothelial cells on Matrigel. We obtained the following evidence that it is vascular endothelial growth factor (VEGF) that mainly mediates the angiogenic activities of AGE. Glucose and other reducing sugars can react nonenzymatically with the amino groups of proteins to form reversible Schiff bases and, then, Amadori products. These early glycation products undergo further complex reactions such as rearrangement, dehydration, and condensation to become irreversibly crosslinked, heterogeneous fluorescent derivatives termed advanced glycation end products (AGE) 1 (1). The formation and accumulation of AGE in various tissues have been known to progress during normal aging and at an extremely accelerated rate in diabetes mellitus. This has been implicated in the development of diabetic micro-and macro-vascular complications (1), which may account for the disabilities and high mortality rate in patients with this disease (2).Microvessels are composed of only two types of cells, endothelial cells and pericytes, and have been known to show both functional and structural abnormalities during prolonged diabetic exposure, resulting in the deleterious effects on the organs that they supply (3-5). Using pericyte-endothelial cell co-culture systems, we have shown previously that pericytes can not only regulate the growth but also preserve the prostacyclin-producing ability and protect against lipid peroxide-induced injury of endothelial cells (6). This has provided a basis for understanding how diabetic retinopathy develops consequent to "pericyte loss," the earliest histopathological hallmark in diabetic retinopathy (5, 7).Recently, we have found that AGE exert a growth inhibitory effect and a cell type-specific immediate toxicity on pericytes through interactions with their receptor for AGE (RAGE), a cell surface receptor belonging to the immunoglobulin superfamily (8), and have proposed a novel mechanism for pericyte loss (9). The AGE-induced, RAGE-mediated decrease in pericyte number would then indirectly cause angiogenesis (6,9).In the present study, we investigated the effects of AGE on the growth and tube formation of human skin microvascular endothelial cells, the key steps of angiogenesis. We demonstrate that AGE exert angiogenic activities directly on microvasc...

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“…This protein, vascular endothelial cell growth factor (VEGF), has been implicated in the stimulation of normal angiogenesis and the increased capillary formation that characterizes proliferative diabetic retinopathy (5). VEGF is also considered to be critical for the angiogenesis that underlies tumor metastasis (6,7).…”

mentioning

confidence: 99%

Vasoactive Peptides Modulate Vascular Endothelial Cell Growth Factor Production and Endothelial Cell Proliferation and Invasion

Pedram¹,

Razandi²,

Hu³

et al. 1997

Journal of Biological Chemistry

177

117

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Vascular Endothelial Growth Factor in Ocular Fluid of Patients with Diabetic Retinopathy and Other Retinal Disorders

Abstract: Our data suggest that VEGF plays a major part in mediating active intraocular neovascularization in patients with ischemic retinal diseases, such as diabetic retinopathy and retinal-vein occlusion.

Cited by 3,388 publications

References 28 publications

Expression and function of vascular endothelial growth factor receptor-1 on human colorectal cancer cells

Expression and function of vascular endothelial growth factor receptor-1 on human colorectal cancer cells

Advanced Glycation End Products-driven Angiogenesis in Vitro

Vasoactive Peptides Modulate Vascular Endothelial Cell Growth Factor Production and Endothelial Cell Proliferation and Invasion

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