Gold Nanoparticles Inhibit VEGF<sub>165</sub>-Induced Migration and Tube Formation of Endothelial Cells via the Akt Pathway

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  • Yunlong Pan
    Department of General Surgery, The First Affiliated Hospital of Jinan University, Guangzhou 510632, China
  • Qing Wu
    Department of General Surgery, The First Affiliated Hospital of Jinan University, Guangzhou 510632, China
  • Li Qin
    Department of Histology and Embryology, Medical School of Jinan University, Guangzhou 510632, China
  • Jiye Cai
    Department of Chemistry, Life Science and Technology School of Jinan University, Guangzhou 510632, China
  • Bin Du
    Department of Pathology, Medical School of Jinan University, Guangzhou 510632, China

Description

<jats:p>The early stages of angiogenesis can be divided into three steps: endothelial cell proliferation, migration, and tube formation. Vascular endothelial growth factor (VEGF) is considered the most important proangiogenic factor; in particular, VEGF<jats:sub>165</jats:sub>plays a critical role in angiogenesis. Here, we evaluated whether gold nanoparticles (AuNPs) could inhibit the VEGF<jats:sub>165</jats:sub>-induced human umbilical vein endothelial cell (HUVEC) migration and tube formation. AuNPs and VEGF<jats:sub>165</jats:sub>were coincubated overnight at 4°C, after which the effects on cell migration and tube formation were assessed. Cell migration was assessed using a modified wound-healing assay and a transwell chamber assay; tube formation was assessed using a capillary-like tube formation assay and a chick chorioallantoic membrane (CAM) assay. We additionally detected the cell surface morphology and ultrastructure using atomic force microscopy (AFM). Furthermore, Akt phosphorylation downstream of VEGFR-2/PI3K in HUVECs was determined in a Western blot analysis. Our study demonstrated that AuNPs significantly inhibited VEGF<jats:sub>165</jats:sub>-induced HUVEC migration and tube formation by affecting the cell surface ultrastructure, cytoskeleton and might have inhibited angiogenesis via the Akt pathway.</jats:p>

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