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Published 20 June 2005. doi:10.1083/jcb.200411155
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 169, Number 6, 941-952
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Article

 Conditional knockout of focal adhesion kinase in endothelial cells reveals its role in angiogenesis and vascular development in late embryogenesis

Tang-Long Shen1, Ann Y.-J. Park1, Ana Alcaraz2, Xu Peng1, Ihnkyung Jang3,4, Pandelakis Koni5, Richard A. Flavell5, Hua Gu3,4, and Jun-Lin Guan1

1 Department of Molecular Medicine, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853
2 Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853
3 Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852
4 Department of Microbiology, Columbia University College of Physicians and Surgeons, New York, NY 10032
5 Section of Immunobiology, Yale University School of Medicine, Howard Hughes Medical Institute, New Haven, CT 06520

Correspondence to J.-L. Guan: jg19{at}cornell.edu

Focal adhesion kinase (FAK) is a critical mediator of signal transduction by integrins and growth factor receptors in a variety of cells including endothelial cells (ECs). Here, we describe EC-specific knockout of FAK using a Cre-loxP approach. In contrast to the total FAK knockout, deletion of FAK specifically in ECs did not affect early embryonic development including normal vasculogenesis. However, in late embryogenesis, FAK deletion in the ECs led to defective angiogenesis in the embryos, yolk sac, and placenta, impaired vasculature and associated hemorrhage, edema, and developmental delay, and late embryonic lethal phenotype. Histologically, ECs and blood vessels in the mutant embryos present a disorganized, detached, and apoptotic appearance. Consistent with these phenotypes, deletion of FAK in ECs isolated from the floxed FAK mice led to reduced tubulogenesis, cell survival, proliferation, and migration in vitro. Together, these results strongly suggest a role of FAK in angiogenesis and vascular development due to its essential function in the regulation of multiple EC activities.

P. Koni's present address is Medical College of Georgia, Augusta, GA 30912.

T.-L. Shen's present address is National Taiwan University, Taipei, Taiwan 106.

Abbreviations used in this paper: CFKO, conditional FAK knockout; EC, endothelial cell; MEF, mouse embryonic fibroblast; PECAM-1, platelet-endothelial cell adhesion molecule-1.


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