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Related Collections Hemostasis, Thrombosis, and Vascular Biology Gene Therapy Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 June 2002, Vol. 99, No. 12, pp. 4434-4442 HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Adenovirus encoding vascular endothelial growth factor-D induces tissue-specific vascular patterns in vivo Tatiana V. Byzova, Corey K. Goldman, Jurek Jankau, Juhua Chen, Gustavo Cabrera, Marc G. Achen, Steven A. Stacker, Kevin A. Carnevale, Maria Siemionow, Steven R. Deitcher, and Paul E. DiCorleto From the Departments of Molecular Cardiology and Cardiology, Vascular Medicine, Cell Biology, and Plastic and Reconstructive Surgery, The Cleveland Clinic Foundation, OH; and the Ludwig Institute for Cancer Research, Royal Melbourne Hospital, Victoria, Australia. The capacity of an adenovirus encoding the mature form of vascular endothelial growth factor (VEGF)-D, VEGF-DNC, to induce angiogenesis, lymphangiogenesis, or both was analyzed in 2 distinct in vivo models. We first demonstrated in vitro that VEGF-DNC encoded by the adenovirus (Ad-VEGF-DNC) is capable of inducing endothelial cell proliferation and migration and that the latter response is primarily mediated by VEGF receptor-2 (VEGFR-2). Second, we characterized a new in vivo model for assessing experimental angiogenesis, the rat cremaster muscle, which permits live videomicroscopy and quantitation of functional blood vessels. In this model, a proangiogenic effect of Ad-VEGF-DNC was evident as early as 5 days after injection. Immunohistochemical analysis of the cremaster muscle demonstrated that neovascularization induced by Ad-VEGF-DNC and by Ad-VEGF-A165 (an adenovirus encoding the 165 isoform of VEGF-A) was composed primarily of laminin and VEGFR-2-positive vessels containing red blood cells, thus indicating a predominantly angiogenic response. In a skin model, Ad-VEGF-DNC induced angiogenesis and lymphangiogenesis, as indicated by staining with laminin, VEGFR-2, and VEGFR-3, whereas Ad-VEGF-A165 stimulated the selective growth of blood vessels. These data suggest that the biologic effects of VEGF-D are tissue-specific and dependent on the abundance of blood vessels and lymphatics expressing the receptors for VEGF-D in a given tissue. The capacity of Ad-VEGF-DNC to induce endothelial cell proliferation, angiogenesis, and lymphangiogenesis demonstrates that its potential usefulness for the treatment of coronary artery disease, cerebral ischemia, peripheral vascular disease, restenosis, and tissue edema should be tested in preclinical models. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. R. Somanath, E. S. Kandel, N. Hay, and T. V. Byzova Akt1 Signaling Regulates Integrin Activation, Matrix Recognition, and Fibronectin Assembly J. Biol. Chem., August 3, 2007; 282(31): 22964 - 22976. [Abstract] [Full Text] [PDF] X. Ju, S. Katiyar, C. Wang, M. Liu, X. Jiao, S. Li, J. Zhou, J. Turner, M. P. Lisanti, R. G. Russell, et al. Akt1 governs breast cancer progression in vivo PNAS, May 1, 2007; 104(18): 7438 - 7443. [Abstract] [Full Text] [PDF] B. K. McColl, K. Paavonen, T. Karnezis, N. C. 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	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020