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Blood, 1 September 2008, Vol. 112, No. 5, pp. 1740-1749. Prepublished online as a Blood First Edition Paper on May 12, 2008; DOI 10.1182/blood-2007-08-106302. This Article Full Text (PDF) Supplemental Methods, Tables, and Figures All Versions of this Article: blood-2007-08-106302v1 112/5/1740    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Google Scholar Articles by Ny, A. Articles by Dewerchin, M. PubMed PubMed Citation Articles by Ny, A. Articles by Dewerchin, M. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted August 10, 2007 Accepted March 6, 2008 Role of VEGF-D and VEGFR-3 in developmental lymphangiogenesis, a chemicogenetic study in Xenopus tadpoles Annelii Ny, Marta Koch, Wouter Vandevelde, Martin Schneider, Christian Fischer, Antonio Diez-Juan, Elke Neven, Ilse Geudens, Sunit Maity, Lieve Moons, Stephane Plaisance, Diether Lambrechts, Peter Carmeliet, and Mieke Dewerchin* Department of Transgene Technology and Gene Therapy, VIB, K.U.Leuven, Leuven, Belgium The Center for Transgene Technology and Gene Therapy (CTG), K.U.Leuven, Leuven, Belgium * Corresponding author; email: mieke.dewerchin{at}med.kuleuven.be. The importance of the lymphangiogenic factor VEGF-D and its receptor VEGFR-3 in early lymphatic development remains largely unresolved. We therefore investigated their role in Xenopus laevis tadpoles, a small animal model allowing chemicogenetic dissection of developmental lymphangiogenesis. Single morpholino antisense oligo knockdown of VEGF-D did not affect lymphatic commitment, but transiently impaired lymphatic endothelial cell (LEC) migration. Notably, combined knockdown of VEGF-D with VEGF-C at suboptimal morpholino concentrations, resulted in more severe migration defects and lymphedema formation than the corresponding single knockdowns. Knockdown of VEGFR-3 or treatment with the VEGFR-3 inhibitor MAZ51 similarly impaired lymph vessel formation and function and caused pronounced edema. VEGFR-3 silencing by morpholino knockdown, MAZ51 treatment, or VEGF-C/D double knockdown also resulted in dilation and dysfunction of the lymph heart. These findings document a critical role of VEGFR-3 in embryonic lymphatic development and function, and reveal a previously unrecognized modifier role of VEGF-D in the regulation of embryonic lymphangiogenesis in frog embryos. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: VEGF-D: a modifier of embryonic lymphangiogenesis Terhi Karpanen and Kari Alitalo Blood 2008 112: 1547-1548. [Full Text] [PDF]

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