Cutaneomucosal venous malformations (VMCMs) are rare inherited disorders caused by mutations in the tyrosine receptor kinase TIE-2. Although thought to function in vascular development and stability, exactly how TIE-2 mutations cause VMCMs is unclear, partly because Tie-2−/− mice are embryonic lethal owing to heart defects. Gjini et al. now report that a tie-2 loss-of-function zebrafish mutant is viable into adulthood. Unlike mice, the function of Tie-2 in zebrafish seems to be redundant to that of Tie-1 during early heart development, although both proteins are required for endocardial-myocardial interactions at later stages. In addition, testing of statins in the tie-2 zebrafish mutant suggests that these drugs act by reducing endothelial cell-cell contacts in newly forming brain vessels.
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IN THIS ISSUE| 01 January 2011
Venous malformations: TIEing genotype to phenotype in zebrafish
Online Issn: 1754-8411
Print Issn: 1754-8403
© 2011. Published by The Company of Biologists Ltd
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.
Dis Model Mech (2011) 4 (1): 1.
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Venous malformations: TIEing genotype to phenotype in zebrafish. Dis Model Mech 1 January 2011; 4 (1): 1. doi:
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