Table of Contents Author Guidelines Submit a Manuscript
BioMed Research International
Volume 2014, Article ID 418624, 11 pages
http://dx.doi.org/10.1155/2014/418624
Research Article

Gold Nanoparticles Inhibit VEGF165-Induced Migration and Tube Formation of Endothelial Cells via the Akt Pathway

1Department of General Surgery, The First Affiliated Hospital of Jinan University, Guangzhou 510632, China
2Department of Histology and Embryology, Medical School of Jinan University, Guangzhou 510632, China
3Department of Chemistry, Life Science and Technology School of Jinan University, Guangzhou 510632, China
4Department of Pathology, Medical School of Jinan University, Guangzhou 510632, China
5Division of Clinic Pathology, The First Affiliated Hospital of Jinan University, Guangzhou 510632, China

Received 5 February 2014; Revised 27 April 2014; Accepted 28 April 2014; Published 1 June 2014

Academic Editor: Gagan Deep

Copyright © 2014 Yunlong Pan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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, VEGF165 plays a critical role in angiogenesis. Here, we evaluated whether gold nanoparticles (AuNPs) could inhibit the VEGF165-induced human umbilical vein endothelial cell (HUVEC) migration and tube formation. AuNPs and VEGF165 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 VEGF165-induced HUVEC migration and tube formation by affecting the cell surface ultrastructure, cytoskeleton and might have inhibited angiogenesis via the Akt pathway.