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© The Rockefeller University Press, 0021-9525/1997//257 $5.00
The Journal of Cell Biology, Volume 139, Number 1, , 1997 257-264

Article

Induction of the Angiogenic Phenotype by Hox D3



Nancy Boudreau*, Catherine Andrews*, Anabella Srebrow{ddagger}, Ali Ravanpay{ddagger}, and David A. Cheresh*

* Department of Immunology and Vascular Biology, The Scripps Research Institute, La Jolla, California 92037; and {ddagger} Life Sciences Division, Ernest Orlando Lawrence Berkeley National Laboratory, Berkeley, California 94720

Angiogenesis is characterized by distinct phenotypic changes in vascular endothelial cells (EC). Evidence is provided that the Hox D3 homeobox gene mediates conversion of endothelium from the resting to the angiogenic/invasive state. Stimulation of EC with basic fibroblast growth factor (bFGF) resulted in increased expression of Hox D3, integrin {alpha}vβ3, and the urokinase plasminogen activator (uPA). Hox D3 antisense blocked the ability of bFGF to induce uPA and integrin {alpha}vβ3 expression, yet had no effect on EC cell proliferation or bFGF-mediated cyclin D1 expression. Expression of Hox D3, in the absence of bFGF, resulted in enhanced expression of integrin {alpha}vβ3 and uPA. In fact, sustained expression of Hox D3 in vivo on the chick chorioallantoic membrane retained EC in this invasive state and prevented vessel maturation leading to vascular malformations and endotheliomas. Therefore, Hox D3 regulates EC gene expression associated with the invasive stage of angiogenesis.

Abbreviations used in this paper: bFGF, basic fibroblast growth factor; BM, basement membrane; CAM, chorioallantoic membrane; EC, vascular endothelial cells; HUVEC, human umbilical vein endothelial cells; uPA, urokinase plasminogen activator.

Address all correspondence to Nancy Boudreau, Department of Anatomy, Medical College of Virginia, 1101 E. Marshall Street, Richmond, VA 23298. Tel.: (804) 828-7887. Fax: (804) 828-9477. E-mail: nboudrea @nsc.vcu.edu


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