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Antiangiogenic Properties of Gold Nanoparticles

Authors' Affiliations: Departments of ¹ Biochemistry and Molecular Biology, and ² Biomedical Engineering, Mayo Clinic Cancer Center, Rochester, Minnesota, ³ Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts; and ⁴ Wake Forest Institute for Regenerative Medicine, Winston-Salem, North Carolina

Requests for reprints: Debabrata Mukhopadhyay, Department of Biochemistry and Molecular Biology, Gugg 1401A, Mayo Clinic Foundation, 200 First Street, Southwest Rochester, MN 55905. Phone: 507-538-3581; Fax: 507-284-1767; E-mail: mukhopadhyay.debabrata{at}mayo.edu.

Here, we report an intrinsic property of gold nanoparticles (nanogold): they can interact selectively with heparin-binding glycoproteins and inhibit their activity. Gold nanoparticles specifically bound vascular permeability factor/vascular endothelial growth factor (VPF/VEGF)-165 and basic fibroblast growth factor, two endothelial cell mitogens and mediators of angiogenesis resulting in inhibition of endothelial/fibroblast cell proliferation in vitro and VEGF-induced permeability as well as angiogenesis in vivo. In contrast, nanogold did not inhibit VEGF-121 or epidermal growth factor, two non–heparin-binding growth factors, mediated cell proliferation. Gold nanoparticles significantly inhibited VEGF receptor-2 phosphorylation, intracellular calcium release, and migration and RhoA activation in vitro. These results report for the first time a novel property of gold nanoparticles to bind heparin-binding proteins and thereby inhibit their subsequent signaling events.

Key Words: gold nanoparticles • VEGF/VPF • Heparin binding growth factors • angiogenesis

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