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Molecular and Cellular Biology, April 2007, p. 2687-2697, Vol. 27, No. 7
0270-7306/07/$08.00+0     doi:10.1128/MCB.00493-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

TAL-1/SCL and Its Partners E47 and LMO2 Up-Regulate VE-Cadherin Expression in Endothelial Cells ^,

Virginie Deleuze,^1,2,¶ Elias Chalhoub,^1,2,,¶ Rawan El-Hajj,^1,2 Christiane Dohet,^1,2 Mikaël Le Clech,^1,2, Pierre-Olivier Couraud,^3,4 Philippe Huber,⁵ and Danièle Mathieu^1,2*

Institut de Génétique Moléculaire de Montpellier CNRS, UMR5535, Montpellier, France,¹ Université de Montpellier 2, Montpellier, France,² Institut Cochin, INSERM/CNRS, Paris, France,³ Université Paris 5, Paris, France,⁴ CEA, INSERM, Grenoble, France⁵

Received 21 March 2006/ Returned for modification 20 May 2006/ Accepted 2 January 2007

The basic helix-loop-helix TAL-1/SCL essential for hematopoietic development is also required during vascular development for embryonic angiogenesis. We reported that TAL-1 acts positively on postnatal angiogenesis by stimulating endothelial morphogenesis. Here, we investigated the functional consequences of TAL-1 silencing in human primary endothelial cells. We found that TAL-1 knockdown caused the inhibition of in vitro tubulomorphogenesis, which was associated with a dramatic reduction in vascular endothelial cadherin (VE-cadherin) at intercellular junctions. Consistently, silencing of TAL-1 as well as of its cofactors E47 and LMO2 down-regulated VE-cadherin at both the mRNA and the protein level. Endogenous VE-cadherin transcription could be activated in nonendothelial HEK-293 cells by the sole concomitant ectopic expression of TAL-1, E47, and LMO2. Transient transfections in human primary endothelial cells derived from umbilical vein (HUVECs) demonstrated that VE-cadherin promoter activity was dependent on the integrity of a specialized E-box associated with a GATA motif and was maximal with the coexpression of the different components of the TAL-1 complex. Finally, chromatin immunoprecipitation assays showed that TAL-1 and its cofactors occupied the VE-cadherin promoter in HUVECs. Together, these data identify VE-cadherin as a bona fide target gene of the TAL-1 complex in the endothelial lineage, providing a first clue to TAL-1 function in angiogenesis.

Published ahead of print on 22 January 2007.

Supplemental material for this article may be found at http://mcb.asm.org/.

^¶ V. Deleuze and E. Chalhoub contributed equally to the work.

Present address: University of Beirut, Beirut, Lebanon.

Present address: Max Planck Institute for Biochemistry, 82152 Martinsried, Germany.

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