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(American Journal of Pathology. 2000;156:1345-1362.)
© 2000 American Society for Investigative Pathology

Regular Articles

Regulation of Angiogenesis in Vivo by Ligation of Integrin {alpha}5ß1 with the Central Cell-Binding Domain of Fibronectin

Semi Kim*, Kelly Bell*, Shaker A. Mousa{dagger} and Judith A. Varner*

From the Department of Medicine/Cancer Center,*
Cellular and Molecular Medicine East, University of California San Diego, La Jolla, California; and Research and Development Cardiovascular,{dagger}
DuPont Pharmaceuticals, Wilmington, Delaware

Angiogenesis depends on the cooperation of growth factors and cell adhesion events. Although {alpha}v integrins have been shown to play critical roles in angiogenesis, recent studies in {alpha}v-null mice suggest that other adhesion receptors and their ligands also regulate this process. Evidence is now provided that the integrin {alpha}5ß1 and its ligand fibronectin are coordinately up-regulated on blood vessels in human tumor biopsies and play critical roles in angiogenesis, resulting in tumor growth in vivo. Angiogenesis induced by multiple growth factors in chick embryos was blocked by monoclonal antibodies to the cell-binding domain of fibronectin. Furthermore, application of fibronectin or a proteolytic fragment of fibronectin containing the central cell-binding domain to the chick chorioallantoic membrane enhanced angiogenesis in an integrin {alpha}5ß1-dependent manner. Importantly, antibody, peptide, and novel nonpeptide antagonists of integrin {alpha}5ß1 blocked angiogenesis induced by several growth factors but had little effect on angiogenesis induced by vascular endothelial growth factor (VEGF) in both chick embryo and murine models. In fact, these {alpha}5ß1 antagonists inhibited tumor angiogenesis, thereby causing regression of human tumors in animal models. Thus, fibronectin and integrin {alpha}5ß1, like integrin {alpha}vß3, contribute to an angiogenesis pathway that is distinct from VEGF-mediated angiogenesis, yet important for the growth of tumors.




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