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      Vascular endothelial growth factors and vascular permeability

      *

      Cardiovascular Research

      Oxford University Press

      VEGF, Vascular permeability, Calcium, Capillary, Endothelium

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          Abstract

          Vascular endothelial growth factors (VEGFs) are key regulators of permeability. The principal evidence behind how they increase vascular permeability in vivo and in vitro and the consequences of that increase are addressed here. Detailed analysis of the published literature has shown that in vivo and in vitro VEGF-mediated permeability differs in its time course, but has common involvement of many specific signalling pathways, in particular VEGF receptor-2 activation, calcium influx through transient receptor potential channels, activation of phospholipase C gamma and downstream activation of nitric oxide synthase. Pathways downstream of endothelial nitric oxide synthase appear to involve the guanylyl cyclase-mediated activation of the Rho–Rac pathway and subsequent involvement of junctional signalling proteins such as vascular endothelial cadherin and the tight junctional proteins zona occludens and occludin linked to the actin cytoskeleton. The signalling appears to be co-ordinated through spatial organization of the cascade into a signalplex, and arguments for why this may be important are considered. Many proteins have been identified to be involved in the regulation of vascular permeability by VEGF, but still the mechanisms through which these are thought to interact to control permeability are dependent on the experimental system, and a synthesis of existing data reveals that in intact vessels the co-ordination of the pathways is still not understood.

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          Most cited references 124

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          The biology of vascular endothelial growth factor.

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            Vascular endothelial growth factor is a secreted angiogenic mitogen.

            Vascular endothelial growth factor (VEGF) was purified from media conditioned by bovine pituitary folliculostellate cells (FC). VEGF is a heparin-binding growth factor specific for vascular endothelial cells that is able to induce angiogenesis in vivo. Complementary DNA clones for bovine and human VEGF were isolated from cDNA libraries prepared from FC and HL60 leukemia cells, respectively. These cDNAs encode hydrophilic proteins with sequences related to those of the A and B chains of platelet-derived growth factor. DNA sequencing suggests the existence of several molecular species of VEGF. VEGFs are secreted proteins, in contrast to other endothelial cell mitogens such as acidic or basic fibroblast growth factors and platelet-derived endothelial cell growth factor. Human 293 cells transfected with an expression vector containing a bovine or human VEGF cDNA insert secrete an endothelial cell mitogen that behaves like native VEGF.
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              Vascular endothelial growth factor is a potential tumour angiogenesis factor in human gliomas in vivo.

               G Breier,  H Weich,  W Risau (1992)
              Clinical and experimental studies suggest that angiogenesis is a prerequisite for solid tumour growth. Several growth factors with mitogenic or chemotactic activity for endothelial cells in vitro have been described, but it is not known whether these mediate tumour vascularization in vivo. Glioblastoma, the most common and most malignant brain tumour in humans, is distinguished from astrocytoma by the presence of necroses and vascular proliferations. Here we show that expression of an endothelial cell-specific mitogen, vascular endothelial growth factor (VEGF), is induced in astrocytoma cells but is dramatically upregulated in two apparently different subsets of glioblastoma cells. The high-affinity tyrosine kinase receptor for VEGF, flt, although not expressed in normal brain endothelium, is upregulated in tumour endothelial cells in vivo. These observations strongly support the concept that tumour angiogenesis is regulated by paracrine mechanisms and identify VEGF as a potential tumour angiogenesis factor in vivo.
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                Author and article information

                Journal
                Cardiovasc Res
                cvrese
                cardiovascres
                Cardiovascular Research
                Oxford University Press
                0008-6363
                1755-3245
                15 July 2010
                16 April 2010
                16 April 2010
                : 87
                : 2
                : 262-271
                Affiliations
                Microvascular Research Laboratories, Department of Physiology and Pharmacology, School of Veterinary Sciences, Bristol Heart Institute, University of Bristol , Southwell Street, Bristol BS2 8EJ, UK
                Author notes
                [* ]Corresponding author. Tel: +44 117 928 9818; fax: +44 117 928 8151, Email: dave.bates@ 123456bris.ac.uk

                This article is part of the Spotlight Issue on: Microvascular Permeability

                Article
                cvq105
                10.1093/cvr/cvq105
                2895541
                20400620
                Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2010. For permissions please email: journals.permissions@oxfordjournals.org.

                The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that the original authorship is properly and fully attributed; the Journal, Learned Society and Oxford University Press are attributed as the original place of publication with correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org.

                Categories
                Spotlight Reviews

                Cardiovascular Medicine

                vegf, capillary, endothelium, calcium, vascular permeability

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