Mukherjee Priyabrata, Bhattacharya Resham, Wang Ping, Wang Ling, Basu Sujit, Nagy Janice A, Atala Anthony, Mukhopadhyay Debabrata, Soker Shay
Department of Biochemistry, Mayo Clinic Cancer Center, Rochester, Minnesota 55905, USA.
Clin Cancer Res. 2005 May 1;11(9):3530-4. doi: 10.1158/1078-0432.CCR-04-2482.
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.
在此，我们报道了金纳米颗粒（纳米金）的一种内在特性：它们能够与肝素结合糖蛋白选择性相互作用并抑制其活性。金纳米颗粒特异性结合血管通透性因子/血管内皮生长因子（VPF/VEGF）-165和碱性成纤维细胞生长因子，这两种内皮细胞有丝分裂原和血管生成介质，导致体外内皮/成纤维细胞增殖以及体内VEGF诱导的通透性和血管生成受到抑制。相比之下，纳米金并不抑制VEGF-121或表皮生长因子这两种非肝素结合生长因子介导的细胞增殖。金纳米颗粒在体外显著抑制VEGF受体-2磷酸化、细胞内钙释放、迁移以及RhoA激活。这些结果首次报道了金纳米颗粒结合肝素结合蛋白并由此抑制其后续信号事件的新特性。
