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      Vascular endothelial growth factor receptor-2 in macular oedema with retinal vein occlusion.

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          Abstract

          To evaluate the relationships among vitreous fluid levels of soluble vascular endothelial growth factor receptor-2 (sVEGFR-2), vascular endothelial growth factor (VEGF), and the severity of macular oedema secondary to branch retinal vein occlusion (BRVO).

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          VEGF-A stimulates ADAM17-dependent shedding of VEGFR2 and crosstalk between VEGFR2 and ERK signaling.

          Steven Swendeman, Karen Mendelson, Gisela Weskamp … (2008)
          Vascular endothelial growth factor (VEGF)-A and the VEGF receptors are critical for regulating angiogenesis during development and homeostasis and in pathological conditions, such as cancer and proliferative retinopathies. Most effects of VEGF-A are mediated by the VEGFR2 and its coreceptor, neuropilin (NRP)-1. Here, we show that VEGFR2 is shed from cells by the metalloprotease disintegrin ADAM17, whereas NRP-1 is released by ADAM10. VEGF-A enhances VEGFR2 shedding by ADAM17 but not shedding of NRP-1 by ADAM10. VEGF-A activates ADAM17 via the extracellular signal-regulated kinase (ERK) and mitogen-activated protein kinase pathways, thereby also triggering shedding of other ADAM17 substrates, including tumor necrosis factor alpha, transforming growth factor alpha, heparin-binding epidermal growth factor-like growth factor, and Tie-2. Interestingly, an ADAM17-selective inhibitor shortens the duration of VEGF-A-stimulated ERK phosphorylation in human umbilical vein endothelial cells, providing evidence for an ADAM17-dependent crosstalk between the VEGFR2 and ERK signaling. Targeting the sheddases of VEGFR2 or NRP-1 might offer new opportunities to modulate VEGF-A signaling, an already-established target for treatment of pathological neovascularization.
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            Multivariate analyses of inflammatory cytokines in eyes with branch retinal vein occlusion: relationships to bevacizumab treatment.

            Yoshitsugu Inoue, T Funakoshi, Keiko Yakura … (2011)
            To characterize the differential expression of intraocular inflammatory cytokines in eyes with branch retinal vein occlusion (BRVO) and to assess their roles as prognostic determinants of BRVO. A prospective cohort study of 38 eyes with BRVO. Aqueous humor samples were collected just before the intravitreal injection of bevacizumab and were assessed for 18 cytokines, chemokines, and growth factors. For control, aqueous humor was collected from 28 eyes before cataract surgery. In the aqueous of eyes with BRVO, the IL-23, IL-8, IL-6, IL-15, IL-12, and IL-17 levels were significantly higher than that in control eyes. Pretreatment visual acuity was significantly correlated with the concentrations of IL-8, IL-10, IL-2, IL-1β, IL-5, IL-6, IL-23, IL-4, MCP-1, IL-1α, IL-12, IL-13, IFN-γ, and IL-15. The pretreatment nonperfused area (NPA) was significantly correlated with the concentrations of IL-8, IL-2, MCP-1, and IL-6. Logistic regression analyses revealed significant associations between the BRVO and the concentrations of IL-8, IL-23, IL-12, IL-15, IL-10, IL-1β, and IL-13. IL-8 had the highest odds ratio (OR) and was significantly associated with NPA, central retinal thickness (CRT), and visual acuity. Bevacizumab treatment significantly improved visual acuity and CRT after 1 month. Refractoriness to bevacizumab (defined as CRT recovery 1 month after treatment by <90%) was significantly associated with the IL-12 level. Of the induced cytokines in eyes with BRVO, IL-8 was the most significantly associated with the disease parameters of BRVO. IL-12 is most likely a factor that blocks the effect of bevacizumab treatment. (www.umin.ac.jp/ctr number, UMIN000003854.).
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              Role of soluble vascular endothelial growth factor receptor-2 in macular oedema with central retinal vein occlusion.

              Hideharu Funatsu, Hidetaka Noma, Tatsuya Mimura … (2011)
              To measure soluble vascular endothelial growth factor receptor-2 (sVEGFR-2) in the vitreous fluid of patients with central retinal vein occlusion (CRVO) and macular oedema or patients with idiopathic macular hole, and to investigate the relation between sVEGFR-2 and vascular endothelial growth factor (VEGF). Vitreous fluid samples were obtained from 44 patients during vitreoretinal surgery (29 patients with CRVO and 15 with macular hole). Then the sVEGFR-2 and VEGF levels were measured by ELISA. Retinal ischaemia was evaluated by measuring the area of capillary nonperfusion on fluorescein angiograms with the public domain Scion Image program. Macular oedema was examined by optical coherence tomography. CRVO patients had significantly higher vitreous levels of sVEGFR-2 (median (IQR): 1200 pg/ml (835-1740)) than macular hole patients (945 pg/ml (691-1292), p=0.042)). They also had significantly higher vitreous VEGF levels (324 pg/ml (114-1218) vs 15.6 pg/ml (15.6-15.6), p<0.001). In CRVO patients, the vitreous level of VEGF was significantly correlated with the severity of macular oedema (ρ=0.50, p=0.008), but the sVEGFR-2 level was not. The product (sVEGFR-2×VEGF) was also significantly correlated with the severity of macular oedema (ρ=0.49, p=0.008). The strength of the association with macular oedema was similar for the product (sVEGFR-2×VEGF) and for VEGF alone. These findings suggest that macular oedema in CRVO patients is more closely related to VEGF than sVEGFR-2.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Ophthalmic Res.
                Title: Ophthalmic research
                Publisher: S. Karger AG
                ISSN (Electronic): 1423-0259
                ISSN (Print): 0030-3747
                Publication date (Electronic): 2012
                Volume: 48
                Issue: 1
                Affiliations
                [1 ] Department of Ophthalmology, Yachiyo Medical Center, Tokyo Women's Medical University, Chiba, Japan. nomahide@tymc.twmu.ac.jp
                Article
                Publisher Item ID: 000336020
                DOI: 10.1159/000336020
                PubMed ID: 22415022
                SO-VID: a1bc4e58-d5d6-4fd9-96b7-3a6a6032cb7f
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