Vitreous levels of vascular endothelial growth factor are not influenced by its serum concentrations in diabetic retinopathy

Burgos, R.; Simó, Rafael; Audı́, Laura; Mateo, Carlos; Mesa, Jordi; Garcia-Ramírez, Marta; Carrascosa, A.

doi:10.1007/s001250050794

Cited by 94 publications

(71 citation statements)

References 10 publications

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“…Diabetic retinopathy is one of the leading causes of blindness in the United States [Burgos et al, 1997]. DR may be caused by increased retinal vascular permeability, new retinal vessel development, and/or loss of retinal capillaries [Aiello and Wong, 2000].…”

Section: Discussionmentioning

confidence: 99%

Bone morphogenetic protein‐4 enhances vascular endothelial growth factor secretion by human retinal pigment epithelial cells

Vogt

Unda

Yeh

et al. 2006

J of Cellular Biochemistry

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Retinal pigment epithelial (RPE) cells secrete vascular endothelial growth factor (VEGF), a cytokine known to promote angiogenesis. Results from RNase protection assays (RPAs) show that RPE from non-diabetic human donors and from adult retinal pigment epithelium-19 (ARPE-19) cells expressed significant bone morphogenetic protein-4 (BMP-4) message. In addition, ARPE-19 cells cultured in high glucose (25 mM), compared to those in physiological glucose (5.5 mM) released significantly more BMP-4 into the conditioned media (CM). However, the effect of BMP-4 on the release of VEGF by ARPE-19 cells has not been studied. Accordingly, ARPE-19 cells were treated with BMP-4 to determine VEGF secretion. BMP-4 and VEGF levels in the CM and cell lysates were measured by enzyme-linked immunosorbent assay (ELISA). Cells treated with exogenous BMP-4 had higher VEGF in the CM and this treatment effect was dose-and timedependent, while cell lysates had low levels of VEGF. Addition of cycloheximide (CHX) or actinomycin-D (ACT) significantly reduced VEGF secretion from cells treated with BMP-4, suggesting that the BMP-4-induced secretion of VEGF requires new RNA and protein synthesis. Our results suggest that BMP-4 may play a role in the regulation of ocular angiogenesis associated with diabetic retinopathy (DR) by stimulating VEGF release from RPE cells.

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Section: Discussionmentioning

confidence: 99%

Bone morphogenetic protein‐4 enhances vascular endothelial growth factor secretion by human retinal pigment epithelial cells

Vogt

Unda

Yeh

et al. 2006

J of Cellular Biochemistry

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“…[41][42][43][44] Most of the results on VEGF showed a higher level in the vitreous than in the peripheral blood. However, there were few associations between intraocular level and peripheral blood level.…”

Section: Discussionmentioning

confidence: 99%

Involvement of circulating endothelial progenitor cells and vasculogenic factors in the pathogenesis of diabetic retinopathy

Lee

Chae

Kim

2005

Eye

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“…Undoubtedly VEGF is one such factor, and the present study has shown it to be responsible for a significant measure of the angiogenic potential in serum from patients with proliferative retinopathy. High levels of VEGF have been identified in ocular fluids of diabetic patients (28), and while it appears that serum VEGF does not influence intraocular concentrations (29), it is not known whether the converse is also true. Although two reports have suggested no correlation between retinopathy and serum VEGF (30,31), other studies have indicated significantly higher levels of VEGF in the sera of patients with proliferative compared with background retinopathy that correlated with HbA 1c (32).…”

Section: Discussionmentioning

confidence: 99%

Impaired Retinal Angiogenesis in Diabetes

et al. 2005

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Suppression of angiogenesis during diabetes is a recognized phenomenon but is less appreciated within the context of diabetic retinopathy. The current study has investigated regulation of retinal angiogenesis by diabetic serum and determined if advanced glycation end products (AGEs) could modulate this response, possibly via AGE-receptor interactions. A novel in vitro model of retinal angiogenesis was developed and the ability of diabetic sera to regulate this process was quantified. AGE-modified serum albumin was prepared according to a range of protocols, and these were also analyzed along with neutralization of the AGE receptors galectin-3 and RAGE. Retinal ischemia and neovascularization were also studied in a murine model of oxygen-induced proliferative retinopathy (OIR) in wild-type and galectin-3 knockout mice (gal3 ؊/؊ ) after perfusion of preformed AGEs. Serum from nondiabetic patients showed significantly more angiogenic potential than diabetic serum (P < 0.0001) and within the diabetic group, poor glycemic control resulted in more AGEs but less angiogenic potential than tight control (P < 0.01). AGE-modified albumin caused a dose-dependent inhibition of angiogenesis (P < 0.001), and AGE receptor neutralization significantly reversed the AGE-mediated suppression of angiogenesis (P < 0.01). AGE-treated wild-type mice showed a significant increase in inner retinal ischemia and a reduction in neovascularization compared with non-AGE controls (P < 0.001). However, ablation of galectin-3 abolished the AGE-mediated increase in retinal ischemia and restored the neovascular response to that seen in controls. The data suggest a significant suppression of angiogenesis by the retinal microvasculature during diabetes and implicate AGEs and AGEreceptor interactions in its causation. Diabetes 53: 785-794, 2005

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Vitreous levels of vascular endothelial growth factor are not influenced by its serum concentrations in diabetic retinopathy

Cited by 94 publications

References 10 publications

Bone morphogenetic protein‐4 enhances vascular endothelial growth factor secretion by human retinal pigment epithelial cells

Bone morphogenetic protein‐4 enhances vascular endothelial growth factor secretion by human retinal pigment epithelial cells

Involvement of circulating endothelial progenitor cells and vasculogenic factors in the pathogenesis of diabetic retinopathy

Impaired Retinal Angiogenesis in Diabetes

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