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      Proteolytic cleavage of vascular adhesion protein-1 induced by vascular endothelial growth factor in retinal capillary endothelial cells

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          Increased vascular endothelial growth factor levels in the vitreous of eyes with proliferative diabetic retinopathy.

          The vitreous levels of the angiogenic polypeptide vascular endothelial growth factor (also known as vascular permeability factor) were measured and compared in eyes with and without proliferative diabetic retinopathy. Undiluted vitreous samples from 20 eyes were collected at the time of vitrectomy, and vascular endothelial growth factor levels were determined by using a time-resolved immunofluorometric assay. Vitreous vascular endothelial growth factor levels were significantly higher in eyes with proliferative diabetic retinopathy than in eyes without proliferative diabetic retinopathy (P = .006; Wilcoxon Rank Sum Test). The median vitreous concentration in the eyes with proliferative diabetic retinopathy was 29.1 pM and exceeded the known concentration required for the maximal proliferation of vascular endothelial cells in vitro. These data are consistent with vascular endothelial growth factor serving as a physiologically relevant angiogenic factor in proliferative diabetic retinopathy.
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            Determination of vitreous interleukin-1 (IL-1) and tumour necrosis factor (TNF) levels in proliferative diabetic retinopathy.

            We measured interleukin-1 beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha) in the vitreous humour and serum of patients with proliferative diabetic retinopathy (PDR), in order to determine the role of these cytokines in the pathogenesis of the disease. Vitreous and serum samples were collected from 21 patients with PDR who were undergoing pars plana vitrectomy. Control vitreous samples were obtained from cadavers and control serum samples from healthy subjects. The cytokines were measured by enzyme-linked immunosorbent assay. Vitreous IL-1beta and TNF-alpha concentrations in patients with PDR exceeded those of controls (P<0.05), as did serum IL-1beta and TNF-alpha. We suggest that increased vitreous IL-1beta and TNF-alpha levels may play a significant role in the pathogenesis of PDR, which features abnormal cell proliferation and neovascularisation.
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              The regulation of vascular endothelial growth factor-induced microvascular permeability requires Rac and reactive oxygen species.

              Vascular permeability is a complex process involving the coordinated regulation of multiple signaling pathways in the endothelial cell. It has long been documented that vascular endothelial growth factor (VEGF) greatly enhances microvascular permeability; however, the molecular mechanisms controlling VEGF-induced permeability remain unknown. Treatment of microvascular endothelial cells with VEGF led to an increase in reactive oxygen species (ROS) production. ROS are required for VEGF-induced permeability as treatment with the free radical scavenger, N-acetylcysteine, inhibited this effect. Additionally, treatment with VEGF caused ROS-dependent tyrosine phosphorylation of both vascular-endothelial (VE)-cadherin and beta-catenin. Rac1 was required for the VEGF-induced increase in permeability and adherens junction protein phosphorylation. Knockdown of Rac1 inhibited VEGF-induced ROS production consistent with Rac lying upstream of ROS in this pathway. Collectively, these data suggest that VEGF leads to a Rac-mediated generation of ROS, which, in turn, elevates the tyrosine phosphorylation of VE-cadherin and beta-catenin, ultimately regulating adherens junction integrity.
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                Author and article information

                Journal
                Japanese Journal of Ophthalmology
                Jpn J Ophthalmol
                Springer Science and Business Media LLC
                0021-5155
                1613-2246
                March 2018
                February 1 2018
                March 2018
                : 62
                : 2
                : 256-264
                Article
                10.1007/s10384-017-0555-4
                © 2018

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